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Article(id=1207416366160781590, tenantId=1146029695717560320, journalId=1189873630562394117, issueId=1207416365246419268, articleNumber=null, orderNo=null, doi=10.11855/j.issn.0577-7402.2022.09.0926, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=research-article, receivedDate=1636905600000, receivedDateStr=2021-11-15, revisedDate=null, revisedDateStr=null, acceptedDate=1637769600000, acceptedDateStr=2021-11-25, onlineDate=1765800094403, onlineDateStr=2025-12-15, pubDate=1664294400000, pubDateStr=2022-09-28, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1765800094403, onlineIssueDateStr=2025-12-15, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1765800094403, creator=13701087609, updateTime=1765800094403, updator=13701087609, issue=Issue{id=1207416365246419268, tenantId=1146029695717560320, journalId=1189873630562394117, year='2022', volume='47', issue='9', pageStart='851', pageEnd='956', issueExtLink='null', onlineDate='null', pubDate='null', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=0, createTime=1765800094186, creator=13701087609, updateTime=1765800167087, updator=13701087609, preIssue=null, nextIssue=null, ext={EN=IssueExt(id=1207416671069904914, tenantId=1146029695717560320, journalId=1189873630562394117, issueId=1207416365246419268, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1207416671069904915, tenantId=1146029695717560320, journalId=1189873630562394117, issueId=1207416365246419268, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null}, startPage=926, endPage=931, ext={EN=ArticleExt(id=1207416366466965784, articleId=1207416366160781590, tenantId=1146029695717560320, journalId=1189873630562394117, language=EN, title=Research progress on the mechanism of Drp1 in diabetic cardiomyopathy, columnId=1190243275882729994, journalTitle=Medical Journal of Chinese People’s Liberation Army, columnName=Review, runingTitle=null, highlight=null, articleAbstract=

Diabetic cardiomyopathy is one of the chronic irreversible and serious cardiovascular complications in diabetic patients. Recent studies have shown that the mitochondrial dysfunction caused by the disturbance of mitochondrial dynamic balance is closely related to the occurrence of diabetic cardiomyopathy. Dynamin related protein 1 (Drp1) is an important regulator of mitochondrial fission. Studies have shown that increased activity of Drp1 in diabetes cardiomyocytes can lead to increased mitochondrial fission and decreased mitochondrial fusion which leads to mitochondrial dysfunction. Drp1 can lead to the occurrence and development of diabetic cardiomyopathy by inducing oxidative stress, energy metabolism disorders, apoptosis,insulin resistance, and lipotoxicity in cardiomyocytes. In addition, inhibition of Drp1 activity may improve cardiac function in diabetic cardiomyopathy. Therefore, the mechanism of Drp1 in diabetic cardiomyopathy have been reviewed in present paper in order to provide new ideas for the prevention and treatment of diabetic cardiomyopathy and drug development.

, correspAuthors=Bing Wu, Yong-Qing Chen, authorNote=null, correspAuthorsNote=
* Chen Yong-Qing, E-mail: ;
Wu Bing, E-mail:
, copyrightStatement=null, copyrightOwner=null, extLink=null, articleAbsUrl=null, sourceXml=null, magXml=null, pdfUrl=null, pdf=null, pdfFileSize=null, pdfExtLink=null, richHtmlUrl=null, mobilePdfUrl=null, reviewReport=null, pdfFirstPage=null, abstractGraph=null, abstractGraphContent=null, abstractVideo=null, citation=null, cebUrl=null, magXmlContent=null, mapNumber=null, authorCompany=null, fund=null, authors=null, authorsList=Xiao-Gang Song, Bing Wu, Yong-Qing Chen), CN=ArticleExt(id=1207416366966087964, articleId=1207416366160781590, tenantId=1146029695717560320, journalId=1189873630562394117, language=CN, title=Drp1在糖尿病心肌病中的作用机制研究进展, columnId=1190243276029530637, journalTitle=解放军医学杂志, columnName=综述, runingTitle=null, highlight=null, articleAbstract=

糖尿病心肌病是糖尿病患者严重的慢性不可逆心血管并发症之一。近年来研究发现，线粒体动力学平衡紊乱导致的线粒体功能障碍与糖尿病心肌病的发生密切相关。动力相关蛋白1(Drp1)是线粒体分裂的重要调节因子。研究表明，糖尿病心肌细胞中Drp1活性增强可导致线粒体分裂增加、融合减少，从而引起线粒体功能障碍。Drp1通过诱发心肌细胞氧化应激、能量代谢障碍、细胞凋亡、胰岛素抵抗和脂毒性，导致糖尿病心肌病的发生发展。此外，抑制Drp1的活性可改善糖尿病心肌病的心脏功能。本文对Drp1在糖尿病心肌病中的作用机制进行综述，以期为糖尿病心肌病的防治和药物研发提供新思路。

, correspAuthors=吴冰, 陈永清, authorNote=null, correspAuthorsNote=
陈永清，E-mail：;
吴冰，E-mail：
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宋小刚，硕士研究生，主要从事糖尿病心肌病发病机制方面的研究

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宋小刚，硕士研究生，主要从事糖尿病心肌病发病机制方面的研究

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宋小刚，硕士研究生，主要从事糖尿病心肌病发病机制方面的研究

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articleId=1207416366160781590, language=CN, orderNo=5, keyword=损伤机制)], refs=[Reference(id=1207416371735011715, tenantId=1146029695717560320, journalId=1189873630562394117, articleId=1207416366160781590, doi=null, pmid=null, pmcid=null, year=2018, volume=138, issue=null, pageStart=271, pageEnd=281, url=null, language=null, rfNumber=[1], rfOrder=0, authorNames=Cho NH, Shaw JE, Karuranga S, journalName=Diabetes Res Clin Pract, refType=null, unstructuredReference=Cho NH, Shaw JE, Karuranga S, et al. IDF Diabetes Atlas: Global estimates of diabetes prevalence for 2017 and projections for 2045[J]. Diabetes Res Clin Pract, 2018, 138: 271-281., articleTitle=IDF Diabetes Atlas: Global estimates of diabetes prevalence for 2017 and projections for 2045, refAbstract=null), Reference(id=1207416371835675017, tenantId=1146029695717560320, journalId=1189873630562394117, articleId=1207416366160781590, doi=null, pmid=null, pmcid=null, year=2019, volume=9, issue=null, pageStart=1857, pageEnd=null, url=null, language=null, rfNumber=[2], rfOrder=1, authorNames=Teodoro JS, Nunes S, Rolo AP, journalName=Front Physiol, refType=null, unstructuredReference=Teodoro JS, Nunes S, Rolo AP, et al. Therapeutic options targeting oxidative stress, mitochondrial dysfunction and inflammation to hinder the progression of vascular complications of diabetes[J]. Front Physiol, 2019, 9: 1857., articleTitle=Therapeutic options targeting oxidative stress, mitochondrial dysfunction and inflammation to hinder the progression of vascular complications of diabetes, refAbstract=null), Reference(id=1207416371919561103, tenantId=1146029695717560320, journalId=1189873630562394117, articleId=1207416366160781590, doi=null, pmid=null, pmcid=null, year=2019, volume=124, issue=8, pageStart=1160, pageEnd=1162, url=null, language=null, rfNumber=[3], rfOrder=2, authorNames=Dillmann WH, journalName=Circ Res, refType=null, unstructuredReference=Dillmann WH. Diabetic cardiomyopathy[J]. Circ Res, 2019, 124(8): 1160-1162., articleTitle=Diabetic cardiomyopathy, refAbstract=null), Reference(id=1207416372020224402, tenantId=1146029695717560320, journalId=1189873630562394117, articleId=1207416366160781590, doi=null, pmid=null, pmcid=null, year=2020, volume=21, issue=14, pageStart=4962, pageEnd=null, url=null, language=null, rfNumber=[4], rfOrder=3, authorNames=Bhagani H, Nasser SA, Dakroub A, journalName=Int J Mol Sci, refType=null, unstructuredReference=Bhagani H, Nasser SA, Dakroub A, et al. The mitochondria:a target of polyphenols in the treatment of diabetic cardiomyopathy[J]. Int J Mol Sci, 2020, 21(14): 4962., articleTitle=The mitochondria:a target of polyphenols in the treatment of diabetic cardiomyopathy, refAbstract=null), Reference(id=1207416372104110487, tenantId=1146029695717560320, journalId=1189873630562394117, articleId=1207416366160781590, doi=null, pmid=null, pmcid=null, year=2019, volume=20, issue=11, pageStart=2833, pageEnd=null, url=null, language=null, rfNumber=[5], rfOrder=4, authorNames=Zamora M, Villena JA, journalName=Int J Mol Sci, refType=null, unstructuredReference=Zamora M, Villena JA. Contribution of impaired insulin signaling to the pathogenesis of diabetic cardiomyopathy[J]. Int J Mol Sci, 2019, 20(11): 2833., articleTitle=Contribution of impaired insulin signaling to the pathogenesis of diabetic cardiomyopathy, refAbstract=null), Reference(id=1207416372196385180, tenantId=1146029695717560320, journalId=1189873630562394117, articleId=1207416366160781590, doi=null, pmid=null, pmcid=null, year=2020, volume=45, issue=3, pageStart=323, pageEnd=329, url=null, language=null, rfNumber=[6], rfOrder=5, authorNames=Bai CY, Weng ZY, Xiao C, journalName=Med J Chin PLA, refType=null, unstructuredReference=Bai CY, Weng ZY, Xiao C, et al. Research progress on the relationship of mitochondrial dysfunction to diabetic vascular complications[J]. Med J Chin PLA, 2020, 45(3): 323-329., articleTitle=Research progress on the relationship of mitochondrial dysfunction to diabetic vascular complications, refAbstract=null), Reference(id=1207416372309631396, tenantId=1146029695717560320, journalId=1189873630562394117, articleId=1207416366160781590, doi=null, pmid=null, pmcid=null, year=2020, volume=45, issue=3, pageStart=323, pageEnd=329, url=null, language=null, rfNumber=[6], rfOrder=6, authorNames=白春昀, 翁稚颖, 肖创, journalName=解放军医学杂志, refType=null, unstructuredReference=[白春昀, 翁稚颖, 肖创, 等. 线粒体功能障碍与糖尿病血管并发症关系研究进展[J]. 解放军医学杂志, 2020, 45(3): 323-329.], articleTitle=线粒体功能障碍与糖尿病血管并发症关系研究进展, refAbstract=null), Reference(id=1207416372393517484, tenantId=1146029695717560320, journalId=1189873630562394117, articleId=1207416366160781590, doi=null, pmid=null, pmcid=null, year=2020, volume=45, issue=12, pageStart=1294, pageEnd=1298, url=null, language=null, rfNumber=[7], rfOrder=7, authorNames=Guo Z, Fan D, Tang QZ, journalName=Med J Chin PLA, refType=null, unstructuredReference=Guo Z, Fan D, Tang QZ. Research progress on the mechanism of action of reactive oxygen species in diabetic cardiomyopathy[J]. Med J Chin PLA, 2020, 45(12): 1294-1298., articleTitle=Research progress on the mechanism of action of reactive oxygen species in diabetic cardiomyopathy, refAbstract=null), Reference(id=1207416372502569396, tenantId=1146029695717560320, journalId=1189873630562394117, articleId=1207416366160781590, doi=null, pmid=null, pmcid=null, year=2020, volume=45, issue=12, pageStart=1294, pageEnd=1298, url=null, language=null, rfNumber=[7], rfOrder=8, authorNames=郭振, 樊迪, 唐其柱, journalName=解放军医学杂志, refType=null, unstructuredReference=[郭振, 樊迪, 唐其柱. 活性氧在糖尿病心肌病中的作用机制研究进展[J]. 解放军医学杂志, 2020, 45(12): 1294-1298.], articleTitle=活性氧在糖尿病心肌病中的作用机制研究进展, refAbstract=null), Reference(id=1207416372603232698, tenantId=1146029695717560320, journalId=1189873630562394117, articleId=1207416366160781590, doi=null, pmid=null, pmcid=null, year=2020, volume=71, issue=null, pageStart=100822, pageEnd=null, url=null, language=null, rfNumber=[8], rfOrder=9, authorNames=Morales PE, Arias-Durán C, Ávalos-Guajardo Y, journalName=Mol Aspects Med, refType=null, unstructuredReference=Morales PE, Arias-Durán C, Ávalos-Guajardo Y, et al. Emerging role of mitophagy in cardiovascular physiology and pathology[J]. Mol Aspects Med, 2020, 71: 100822., articleTitle=Emerging role of mitophagy in cardiovascular physiology and pathology, refAbstract=null), Reference(id=1207416372695507391, tenantId=1146029695717560320, journalId=1189873630562394117, articleId=1207416366160781590, doi=null, pmid=null, pmcid=null, year=2019, volume=10, issue=null, pageStart=1404, pageEnd=null, url=null, language=null, rfNumber=[9], rfOrder=10, authorNames=Qiu ZL, Wei Y, Song QQ, journalName=Front Pharmacol, refType=null, unstructuredReference=Qiu ZL, Wei Y, Song QQ, et al. The role of myocardial mitochondrial quality control in heart failure[J]. Front Pharmacol, 2019, 10: 1404., articleTitle=The role of myocardial mitochondrial quality control in heart failure, refAbstract=null), Reference(id=1207416372787782087, tenantId=1146029695717560320, journalId=1189873630562394117, articleId=1207416366160781590, doi=null, pmid=null, pmcid=null, year=2019, volume=316, issue=5, pageStart=C583, pageEnd=C604, url=null, language=null, rfNumber=[10], rfOrder=11, authorNames=Adaniya SM, Jin O, Cypress MW, journalName=Am J Physiol Cell Physiol, refType=null, unstructuredReference=Adaniya SM, Jin O, Cypress MW, et al. Posttranslational modifications of mitochondrial fission and fusion proteins in cardiac physiology and pathophysiology[J]. Am J Physiol Cell Physiol, 2019, 316(5): C583-C604., articleTitle=Posttranslational modifications of mitochondrial fission and fusion proteins in cardiac physiology and pathophysiology, refAbstract=null), Reference(id=1207416372909416914, tenantId=1146029695717560320, journalId=1189873630562394117, articleId=1207416366160781590, doi=null, pmid=null, pmcid=null, year=2020, volume=142, issue=null, pageStart=138, pageEnd=145, url=null, language=null, rfNumber=[11], rfOrder=12, authorNames=Tong MM, Zablocki D, Sadoshima J, journalName=J Mol Cell Cardiol, refType=null, unstructuredReference=Tong MM, Zablocki D, Sadoshima J. The role of Drp1 in mitophagy and cell death in the heart[J]. J Mol Cell Cardiol, 2020, 142: 138-145., articleTitle=The role of Drp1 in mitophagy and cell death in the heart, refAbstract=null), Reference(id=1207416373010080214, tenantId=1146029695717560320, journalId=1189873630562394117, articleId=1207416366160781590, doi=null, pmid=null, pmcid=null, year=2013, volume=369, issue=23, pageStart=2236, pageEnd=2251, url=null, language=null, rfNumber=[12], rfOrder=13, authorNames=Archer SL, journalName=N Engl J Med, refType=null, unstructuredReference=Archer SL. Mitochondrial dynamics-mitochondrial fission and fusion in human diseases[J]. N Engl J Med, 2013, 369(23):2236-2251., articleTitle=Mitochondrial dynamics-mitochondrial fission and fusion in human diseases, refAbstract=null), Reference(id=1207416374234817000, tenantId=1146029695717560320, journalId=1189873630562394117, articleId=1207416366160781590, doi=null, pmid=null, pmcid=null, year=2018, volume=2018, issue=null, pageStart=7514383, pageEnd=null, url=null, language=null, rfNumber=[13], rfOrder=14, authorNames=Lin HY, Weng SW, Chang YH, journalName=Oxid Med Cell Longev, refType=null, unstructuredReference=Lin HY, Weng SW, Chang YH, et al. The causal role of mitochondrial dynamics in regulating insulin resistance in diabetes: link through mitochondrial reactive oxygen species[J]. Oxid Med Cell Longev, 2018, 2018: 7514383., articleTitle=The causal role of mitochondrial dynamics in regulating insulin resistance in diabetes: link through mitochondrial reactive oxygen species, refAbstract=null), Reference(id=1207416374364840434, tenantId=1146029695717560320, journalId=1189873630562394117, articleId=1207416366160781590, doi=null, pmid=null, pmcid=null, year=2021, volume=null, issue=null, pageStart=null, pageEnd=null, url=null, language=null, rfNumber=[14], rfOrder=15, authorNames=Deshpande OA, Mohiuddin SS, journalName=Biochemistry, oxidative phosphorylation, refType=null, unstructuredReference=Deshpande OA, Mohiuddin SS. Biochemistry, oxidative phosphorylation[M]. StatPearls: StatPearls Publishing, 2021., articleTitle=null, refAbstract=null), Reference(id=1207416374486475258, tenantId=1146029695717560320, journalId=1189873630562394117, articleId=1207416366160781590, doi=null, pmid=null, pmcid=null, year=2019, volume=176, issue=22, pageStart=4302, pageEnd=4318, url=null, language=null, rfNumber=[15], rfOrder=16, authorNames=Nguyen BY, Ruiz-Velasco A, Bui T, journalName=Br J Pharmacol, refType=null, unstructuredReference=Nguyen BY, Ruiz-Velasco A, Bui T, et al. Mitochondrial function in the heart: the insight into mechanisms and therapeutic potentials[J]. Br J Pharmacol, 2019, 176(22): 4302-4318., articleTitle=Mitochondrial function in the heart: the insight into mechanisms and therapeutic potentials, refAbstract=null), Reference(id=1207416374599721474, tenantId=1146029695717560320, journalId=1189873630562394117, articleId=1207416366160781590, doi=null, pmid=null, pmcid=null, year=2020, volume=45, issue=7, pageStart=564, pageEnd=577, url=null, language=null, rfNumber=[16], rfOrder=17, authorNames=Sabouny R, Shutt TE, journalName=Trends Biochem Sci, refType=null, unstructuredReference=Sabouny R, Shutt TE. Reciprocal regulation of mitochondrial fission and fusion[J]. Trends Biochem Sci, 2020, 45(7): 564-577., articleTitle=Reciprocal regulation of mitochondrial fission and fusion, refAbstract=null), Reference(id=1207416374704579083, tenantId=1146029695717560320, journalId=1189873630562394117, articleId=1207416366160781590, doi=null, pmid=null, pmcid=null, year=2018, volume=430, issue=21, pageStart=3873, pageEnd=3891, url=null, language=null, rfNumber=[17], rfOrder=18, authorNames=Berry BJ, Trewin AJ, Amitrano AM, journalName=J Mol Biol, refType=null, unstructuredReference=Berry BJ, Trewin AJ, Amitrano AM, et al. Use the protonmotive force: mitochondrial uncoupling and reactive oxygen species[J]. J Mol Biol, 2018, 430(21): 3873-3891., articleTitle=Use the protonmotive force: mitochondrial uncoupling and reactive oxygen species, refAbstract=null), Reference(id=1207416374842991123, tenantId=1146029695717560320, journalId=1189873630562394117, articleId=1207416366160781590, doi=null, pmid=null, pmcid=null, year=2021, volume=700, issue=null, pageStart=108695, pageEnd=null, url=null, language=null, rfNumber=[18], rfOrder=19, authorNames=Ito H, Kurokawa H, Matsui H, journalName=Arch Biochem Biophys, refType=null, unstructuredReference=Ito H, Kurokawa H, Matsui H. Mitochondrial reactive oxygen species and heme, non-heme iron metabolism[J]. Arch Biochem Biophys, 2021, 700: 108695., articleTitle=Mitochondrial reactive oxygen species and heme, non-heme iron metabolism, refAbstract=null), Reference(id=1207416374952043036, tenantId=1146029695717560320, journalId=1189873630562394117, articleId=1207416366160781590, doi=null, pmid=null, pmcid=null, year=2021, volume=26, issue=23, pageStart=7285, pageEnd=null, url=null, language=null, rfNumber=[19], rfOrder=20, authorNames=Mushtaq I, Bashir Z, Sarwar M, journalName=Molecules, refType=null, unstructuredReference=Mushtaq I, Bashir Z, Sarwar M, et al. N-acetyl cysteine, selenium, and ascorbic acid rescue diabetic cardiac hypertrophy via mitochondrial-associated redox regulators[J]. Molecules, 2021, 26(23): 7285., articleTitle=N-acetyl cysteine, selenium, and ascorbic acid rescue diabetic cardiac hypertrophy via mitochondrial-associated redox regulators, refAbstract=null), Reference(id=1207416375090455074, tenantId=1146029695717560320, journalId=1189873630562394117, articleId=1207416366160781590, doi=null, pmid=null, pmcid=null, year=2021, volume=21, issue=12, pageStart=1000, pageEnd=1011, url=null, language=null, rfNumber=[20], rfOrder=21, authorNames=Chen X, Liang J, Bin W, journalName=Cardiovasc Toxicol, refType=null, unstructuredReference=Chen X, Liang J, Bin W, et al. Anti-hyperlipidemic, anti-inflammatory, and ameliorative effects of DRP1 inhibition in rats with experimentally induced myocardial infarction[J]. Cardiovasc Toxicol, 2021, 21(12): 1000-1011., articleTitle=Anti-hyperlipidemic, anti-inflammatory, and ameliorative effects of DRP1 inhibition in rats with experimentally induced myocardial infarction, refAbstract=null), Reference(id=1207416375203701290, tenantId=1146029695717560320, journalId=1189873630562394117, articleId=1207416366160781590, doi=null, pmid=null, pmcid=null, year=2021, volume=41, issue=1, pageStart=1, pageEnd=5, url=null, language=null, rfNumber=[21], rfOrder=22, authorNames=Mui D, Zhang Y, journalName=J Recept Signal Transduct Res, refType=null, unstructuredReference=Mui D, Zhang Y. Mitochondrial scenario: roles of mitochondrial dynamics in acute myocardial ischemia/reperfusion injury[J]. J Recept Signal Transduct Res, 2021, 41(1): 1-5., articleTitle=Mitochondrial scenario: roles of mitochondrial dynamics in acute myocardial ischemia/reperfusion injury, refAbstract=null), Reference(id=1207416375354696244, tenantId=1146029695717560320, journalId=1189873630562394117, articleId=1207416366160781590, doi=null, pmid=null, pmcid=null, year=2019, volume=9, issue=13, pageStart=3687, pageEnd=3706, url=null, language=null, rfNumber=[22], rfOrder=23, authorNames=Hu L, Ding MG, Tang DS, journalName=Theranostics, refType=null, unstructuredReference=Hu L, Ding MG, Tang DS, et al. Targeting mitochondrial dynamics by regulating Mfn2 for therapeutic intervention in diabetic cardiomyopathy[J]. Theranostics, 2019, 9(13): 3687-3706., articleTitle=Targeting mitochondrial dynamics by regulating Mfn2 for therapeutic intervention in diabetic cardiomyopathy, refAbstract=null), Reference(id=1207416375434388028, tenantId=1146029695717560320, journalId=1189873630562394117, articleId=1207416366160781590, doi=null, pmid=null, pmcid=null, year=2020, volume=13, issue=null, pageStart=1057, pageEnd=1073, url=null, language=null, rfNumber=[23], rfOrder=24, authorNames=Checa J, Aran JM, journalName=J Inflamm Res, refType=null, unstructuredReference=Checa J, Aran JM. Reactive oxygen species: drivers of physiological and pathological processes[J]. J Inflamm Res, 2020, 13: 1057-1073., articleTitle=Reactive oxygen species: drivers of physiological and pathological processes, refAbstract=null), Reference(id=1207416375543439938, tenantId=1146029695717560320, journalId=1189873630562394117, articleId=1207416366160781590, doi=null, pmid=null, pmcid=null, year=2019, volume=21, issue=null, pageStart=101100, pageEnd=null, url=null, language=null, rfNumber=[24], rfOrder=25, authorNames=Goh KY, He L, Song JJ, journalName=Redox Biol, refType=null, unstructuredReference=Goh KY, He L, Song JJ, et al. Mitoquinone ameliorates pressure overload-induced cardiac fibrosis and left ventricular dysfunction in mice[J]. Redox Biol, 2019, 21: 101100., articleTitle=Mitoquinone ameliorates pressure overload-induced cardiac fibrosis and left ventricular dysfunction in mice, refAbstract=null), Reference(id=1207416375627326023, tenantId=1146029695717560320, journalId=1189873630562394117, articleId=1207416366160781590, doi=null, pmid=null, pmcid=null, year=2019, volume=46, issue=null, pageStart=73, pageEnd=90, url=null, language=null, rfNumber=[25], rfOrder=26, authorNames=Adeva-Andany MM, Carneiro-Freire N, Seco-Filgueira M, journalName=Mitochondrion, refType=null, unstructuredReference=Adeva-Andany MM, Carneiro-Freire N, Seco-Filgueira M, et al. Mitochondrial β-oxidation of saturated fatty acids in humans[J]. Mitochondrion, 2019, 46: 73-90., articleTitle=Mitochondrial β-oxidation of saturated fatty acids in humans, refAbstract=null), Reference(id=1207416375719600726, tenantId=1146029695717560320, journalId=1189873630562394117, articleId=1207416366160781590, doi=null, pmid=null, pmcid=null, year=2019, volume=2019, issue=null, pageStart=9324018, pageEnd=null, url=null, language=null, rfNumber=[26], rfOrder=27, authorNames=Feno S, Butera G, Vecellio Reane D, journalName=Oxid Med Cell Longev, refType=null, unstructuredReference=Feno S, Butera G, Vecellio Reane D, et al. Crosstalk between calcium and ROS in pathophysiological conditions[J]. Oxid Med Cell Longev, 2019, 2019: 9324018., articleTitle=Crosstalk between calcium and ROS in pathophysiological conditions, refAbstract=null), Reference(id=1207416375816069729, tenantId=1146029695717560320, journalId=1189873630562394117, articleId=1207416366160781590, doi=null, pmid=null, pmcid=null, year=2020, volume=48, issue=2, pageStart=e133, pageEnd=e140, url=null, language=null, rfNumber=[27], rfOrder=28, authorNames=Piao L, Fang YH, Hamanaka RB, journalName=Crit Care Med, refType=null, unstructuredReference=Piao L, Fang YH, Hamanaka RB, et al. Suppression of superoxide-hydrogen peroxide production at site IQ of mitochondrial complex I attenuates myocardial stunning and improves postcardiac arrest outcomes[J]. Crit Care Med, 2020, 48(2):e133-e140., articleTitle=Suppression of superoxide-hydrogen peroxide production at site IQ of mitochondrial complex I attenuates myocardial stunning and improves postcardiac arrest outcomes, refAbstract=null), Reference(id=1207416375916733032, tenantId=1146029695717560320, journalId=1189873630562394117, articleId=1207416366160781590, doi=null, pmid=null, pmcid=null, year=2020, volume=32, issue=3, pageStart=812, pageEnd=821, url=null, language=null, rfNumber=[28], rfOrder=29, authorNames=Zhou X, Qu YL, Gan GS, journalName=Neurocrit Care, refType=null, unstructuredReference=Zhou X, Qu YL, Gan GS, et al. Cyclosporine A plus ischemic postconditioning improves neurological function in rats after cardiac resuscitation[J]. Neurocrit Care, 2020, 32(3): 812-821., articleTitle=Cyclosporine A plus ischemic postconditioning improves neurological function in rats after cardiac resuscitation, refAbstract=null), Reference(id=1207416375983841905, tenantId=1146029695717560320, journalId=1189873630562394117, articleId=1207416366160781590, doi=null, pmid=null, pmcid=null, year=2019, volume=4, issue=12, pageStart=e127660, pageEnd=null, url=null, language=null, rfNumber=[29], rfOrder=30, authorNames=Kakoki M, Bahnson EM, Hagaman JR, journalName=JCI Insight, refType=null, unstructuredReference=Kakoki M, Bahnson EM, Hagaman JR, et al. Engulfment and cell motility protein 1 potentiates diabetic cardiomyopathy via Rac-dependent and Rac-independent ROS production[J]. JCI Insight, 2019, 4(12): e127660., articleTitle=Engulfment and cell motility protein 1 potentiates diabetic cardiomyopathy via Rac-dependent and Rac-independent ROS production, refAbstract=null), Reference(id=1207416376063533687, tenantId=1146029695717560320, journalId=1189873630562394117, articleId=1207416366160781590, doi=null, pmid=null, pmcid=null, year=2021, volume=2021, issue=null, pageStart=8865762, pageEnd=null, url=null, language=null, rfNumber=[30], rfOrder=31, authorNames=Wu J, Chen H, Qin JH, journalName=Oxid Med Cell Longev, refType=null, unstructuredReference=Wu J, Chen H, Qin JH, et al. Baicalin improves cardiac outcome and survival by suppressing Drp1-mediated mitochondrial fission after cardiac arrest-induced myocardial damage[J]. Oxid Med Cell Longev, 2021, 2021: 8865762., articleTitle=Baicalin improves cardiac outcome and survival by suppressing Drp1-mediated mitochondrial fission after cardiac arrest-induced myocardial damage, refAbstract=null), Reference(id=1207416376164196989, tenantId=1146029695717560320, journalId=1189873630562394117, articleId=1207416366160781590, doi=null, pmid=null, pmcid=null, year=2019, volume=8, issue=10, pageStart=454, pageEnd=null, url=null, language=null, rfNumber=[31], rfOrder=32, authorNames=Kuznetsov AV, Javadov S, Margreiter R, journalName=Antioxidants (Basel), refType=null, unstructuredReference=Kuznetsov AV, Javadov S, Margreiter R, et al. The role of mitochondria in the mechanisms of cardiac ischemia-reperfusion injury[J]. Antioxidants (Basel), 2019, 8(10): 454., articleTitle=The role of mitochondria in the mechanisms of cardiac ischemia-reperfusion injury, refAbstract=null), Reference(id=1207416376235500165, tenantId=1146029695717560320, journalId=1189873630562394117, articleId=1207416366160781590, doi=null, pmid=null, pmcid=null, year=2019, volume=2019, issue=null, pageStart=3403075, pageEnd=null, url=null, language=null, rfNumber=[32], rfOrder=33, authorNames=Šileikytė J, Forte M, journalName=Oxid Med Cell Longev, refType=null, unstructuredReference=Šileikytė J, Forte M. The mitochondrial permeability transition in mitochondrial disorders[J]. Oxid Med Cell Longev, 2019, 2019: 3403075., articleTitle=The mitochondrial permeability transition in mitochondrial disorders, refAbstract=null), Reference(id=1207416376344552081, tenantId=1146029695717560320, journalId=1189873630562394117, articleId=1207416366160781590, doi=null, pmid=null, pmcid=null, year=2019, volume=39, issue=1, pageStart=BSR20171307, pageEnd=null, url=null, language=null, rfNumber=[33], rfOrder=34, authorNames=Wu W, Liu XX, Han LF, journalName=Biosci Rep, refType=null, unstructuredReference=Wu W, Liu XX, Han LF. Apoptosis of cardiomyocytes in diabetic cardiomyopathy involves overexpression of glycogen synthase kinase-3β[J]. Biosci Rep, 2019, 39(1): BSR20171307., articleTitle=Apoptosis of cardiomyocytes in diabetic cardiomyopathy involves overexpression of glycogen synthase kinase-3β, refAbstract=null), Reference(id=1207416376453603993, tenantId=1146029695717560320, journalId=1189873630562394117, articleId=1207416366160781590, doi=null, pmid=null, pmcid=null, year=2019, volume=10, issue=null, pageStart=1493, pageEnd=null, url=null, language=null, rfNumber=[34], rfOrder=35, authorNames=Ramalingam A, Budin SB, Mohd Fauzi N, journalName=Front Pharmacol, refType=null, unstructuredReference=Ramalingam A, Budin SB, Mohd Fauzi N, et al. AngiotensinⅡ type Ⅰ receptor antagonism attenuates nicotine-induced cardiac remodeling, dysfunction, and aggravation of myocardial ischemia-reperfusion injury in rats[J]. Front Pharmacol, 2019, 10: 1493., articleTitle=AngiotensinⅡ type Ⅰ receptor antagonism attenuates nicotine-induced cardiac remodeling, dysfunction, and aggravation of myocardial ischemia-reperfusion injury in rats, refAbstract=null), Reference(id=1207416376621376163, tenantId=1146029695717560320, journalId=1189873630562394117, articleId=1207416366160781590, doi=null, pmid=null, pmcid=null, year=2020, volume=7, issue=null, pageStart=12, pageEnd=null, url=null, language=null, rfNumber=[35], rfOrder=36, authorNames=Kaludercic N, di Lisa F, journalName=Front Cardiovasc Med, refType=null, unstructuredReference=Kaludercic N, di Lisa F. Mitochondrial ROS formation in the pathogenesis of diabetic cardiomyopathy[J]. Front Cardiovasc Med, 2020, 7: 12., articleTitle=Mitochondrial ROS formation in the pathogenesis of diabetic cardiomyopathy, refAbstract=null), Reference(id=1207416376789148332, tenantId=1146029695717560320, journalId=1189873630562394117, articleId=1207416366160781590, doi=null, pmid=null, pmcid=null, year=2021, volume=128, issue=10, pageStart=1487, pageEnd=1513, url=null, language=null, rfNumber=[36], rfOrder=37, authorNames=Lopaschuk GD, Karwi QG, Tian R, journalName=Circ Res, refType=null, unstructuredReference=Lopaschuk GD, Karwi QG, Tian R, et al. Cardiac energy metabolism in heart failure[J]. Circ Res, 2021, 128(10): 1487-1513., articleTitle=Cardiac energy metabolism in heart failure, refAbstract=null), Reference(id=1207416376894005939, tenantId=1146029695717560320, journalId=1189873630562394117, articleId=1207416366160781590, doi=null, pmid=null, pmcid=null, year=2021, volume=83, issue=null, pageStart=303, pageEnd=330, url=null, language=null, rfNumber=[37], rfOrder=38, authorNames=Chaurasia B, Summers SA, journalName=Annu Rev Physiol, refType=null, unstructuredReference=Chaurasia B, Summers SA. Ceramides in metabolism: key lipotoxic players[J]. Annu Rev Physiol, 2021, 83: 303-330., articleTitle=Ceramides in metabolism: key lipotoxic players, refAbstract=null), Reference(id=1207416377057583803, tenantId=1146029695717560320, journalId=1189873630562394117, articleId=1207416366160781590, doi=null, pmid=null, pmcid=null, year=2020, volume=598, issue=14, pageStart=2977, pageEnd=2993, url=null, language=null, rfNumber=[38], rfOrder=39, authorNames=Nakamura M, Sadoshima J, journalName=J Physiol, refType=null, unstructuredReference=Nakamura M, Sadoshima J. Cardiomyopathy in obesity, insulin resistance and diabetes[J]. J Physiol, 2020, 598(14): 2977-2993., articleTitle=Cardiomyopathy in obesity, insulin resistance and diabetes, refAbstract=null), Reference(id=1207416377166635717, tenantId=1146029695717560320, journalId=1189873630562394117, articleId=1207416366160781590, doi=null, pmid=null, pmcid=null, year=2020, volume=21, issue=17, pageStart=6358, pageEnd=null, url=null, language=null, rfNumber=[39], rfOrder=40, authorNames=Lair B, Laurens C, van den Bosch B, journalName=Int J Mol Sci, refType=null, unstructuredReference=Lair B, Laurens C, van den Bosch B, et al. Novel insights and mechanisms of lipotoxicity-driven insulin resistance[J]. Int J Mol Sci, 2020, 21(17): 6358., articleTitle=Novel insights and mechanisms of lipotoxicity-driven insulin resistance, refAbstract=null), Reference(id=1207416377300853456, tenantId=1146029695717560320, journalId=1189873630562394117, articleId=1207416366160781590, doi=null, pmid=null, pmcid=null, year=2019, volume=63, issue=7, pageStart=e1801322, pageEnd=null, url=null, language=null, rfNumber=[40], rfOrder=41, authorNames=Chang WG, Xiao DD, Ao X, journalName=Mol Nutr Food Res, refType=null, unstructuredReference=Chang WG, Xiao DD, Ao X, et al. Increased dynamin-related protein 1-dependent mitochondrial fission contributes to high-fat-diet-induced cardiac dysfunction and insulin resistance by elevating tafazzin in mouse hearts[J]. Mol Nutr Food Res, 2019, 63(7): e1801322., articleTitle=Increased dynamin-related protein 1-dependent mitochondrial fission contributes to high-fat-diet-induced cardiac dysfunction and insulin resistance by elevating tafazzin in mouse hearts, refAbstract=null), Reference(id=1207416377388933847, tenantId=1146029695717560320, journalId=1189873630562394117, articleId=1207416366160781590, doi=null, pmid=null, pmcid=null, year=2020, volume=182, issue=null, pageStart=114295, pageEnd=null, url=null, language=null, rfNumber=[41], rfOrder=42, authorNames=Maneechote C, Palee S, Kerdphoo S, journalName=Biochem Pharmacol, refType=null, unstructuredReference=Maneechote C, Palee S, Kerdphoo S, et al. Pharmacological inhibition of mitochondrial fission attenuates cardiac ischemia-reperfusion injury in pre-diabetic rats[J]. Biochem Pharmacol, 2020, 182: 114295., articleTitle=Pharmacological inhibition of mitochondrial fission attenuates cardiac ischemia-reperfusion injury in pre-diabetic rats, refAbstract=null), Reference(id=1207416377477014240, tenantId=1146029695717560320, journalId=1189873630562394117, articleId=1207416366160781590, doi=null, pmid=null, pmcid=null, year=2020, volume=9, issue=9, pageStart=2916, pageEnd=null, url=null, language=null, rfNumber=[42], rfOrder=43, authorNames=Agil A, Chayah M, Visiedo L, journalName=J Clin Med, refType=null, unstructuredReference=Agil A, Chayah M, Visiedo L, et al. Melatonin improves mitochondrial dynamics and function in the kidney of zücker diabetic fatty rats[J]. J Clin Med, 2020, 9(9): 2916., articleTitle=Melatonin improves mitochondrial dynamics and function in the kidney of zücker diabetic fatty rats, refAbstract=null), Reference(id=1207416378647225062, tenantId=1146029695717560320, journalId=1189873630562394117, articleId=1207416366160781590, doi=null, pmid=null, pmcid=null, year=2020, volume=8, issue=null, pageStart=467, pageEnd=null, url=null, language=null, rfNumber=[43], rfOrder=44, authorNames=Ma KL, Chen G, Li WH, journalName=Front Cell Dev Biol, refType=null, unstructuredReference=Ma KL, Chen G, Li WH, et al. Mitophagy, mitochondrial homeostasis, and cell fate[J]. Front Cell Dev Biol, 2020, 8: 467., articleTitle=Mitophagy, mitochondrial homeostasis, and cell fate, refAbstract=null), Reference(id=1207416378747888365, tenantId=1146029695717560320, journalId=1189873630562394117, articleId=1207416366160781590, doi=null, pmid=null, pmcid=null, year=2021, volume=46, issue=11, pageStart=1141, pageEnd=1147, url=null, language=null, rfNumber=[44], rfOrder=45, authorNames=Xie D, Li JY, Pei Q, journalName=Med J Chin PLA, refType=null, unstructuredReference=Xie D, Li JY, Pei Q, et al. Research advances in the role and mechanism of mitophagy in stem cells[J]. Med J Chin PLA, 2021, 46(11): 1141-1147., articleTitle=Research advances in the role and mechanism of mitophagy in stem cells, refAbstract=null), Reference(id=1207416378865328887, tenantId=1146029695717560320, journalId=1189873630562394117, articleId=1207416366160781590, doi=null, pmid=null, pmcid=null, year=2021, volume=null, issue=11, pageStart=1141, pageEnd=1147, url=null, language=null, rfNumber=[44], rfOrder=46, authorNames=谢丹, 李婧媛, 裴琴, journalName=解放军医学杂志, refType=null, unstructuredReference=[谢丹, 李婧媛, 裴琴, 等. 线粒体自噬在干细胞中的作用及其机制研究进展[J]. 解放军医学杂志, 2021, 46(11): 1141-1147.], articleTitle=线粒体自噬在干细胞中的作用及其机制研究进展, refAbstract=null), Reference(id=1207416378949214972, tenantId=1146029695717560320, journalId=1189873630562394117, articleId=1207416366160781590, doi=null, pmid=null, pmcid=null, year=2020, volume=151, issue=null, pageStart=104553, pageEnd=null, url=null, language=null, rfNumber=[45], rfOrder=47, authorNames=Feng ST, Wang ZZ, Yuan YH, journalName=Pharmacol Res, refType=null, unstructuredReference=Feng ST, Wang ZZ, Yuan YH, et al. Dynamin-related protein 1: a protein critical for mitochondrial fission, mitophagy, and neuronal death in Parkinson's disease[J]. Pharmacol Res, 2020, 151: 104553., articleTitle=Dynamin-related protein 1: a protein critical for mitochondrial fission, mitophagy, and neuronal death in Parkinson's disease, refAbstract=null), Reference(id=1207416379041489666, tenantId=1146029695717560320, journalId=1189873630562394117, articleId=1207416366160781590, doi=null, pmid=null, pmcid=null, year=2021, volume=53, issue=10, pageStart=1354, pageEnd=1366, url=null, language=null, rfNumber=[46], rfOrder=48, authorNames=Wei X, Wu YE, Wang W, journalName=Acta Biochim Biophys Sin (Shanghai), refType=null, unstructuredReference=Wei X, Wu YE, Wang W, et al. Decreased dynamin-related protein 1-related mitophagy induces myocardial apoptosis in the aging heart[J]. 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DNA. 脱氧核糖核酸；RNA. 核糖核酸；Cyt C. 细胞色素C；Ⅰ/Ⅱ/Ⅲ/Ⅳ. 线粒体复合体Ⅰ/Ⅱ/Ⅲ/Ⅳ；mPTP. 线粒体通透转换孔；Mfn1. 线粒体融合蛋白1；Mfn2. 线粒体融合蛋白2；Opa1. 视神经萎缩蛋白1；MiD49. 49 kD线粒体动力蛋白；Fis1. 线粒体分裂蛋白1；MiD51. 51 kD线粒体动力蛋白；Drp1. 动力相关蛋白1；Mff. 线粒体裂变因子

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Drp1在糖尿病心肌病中的作用机制研究进展
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宋小刚 1 , 吴冰 2, * , 陈永清 3, *
解放军医学杂志 | 综述 2022,47(9): 926-931
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解放军医学杂志 | 综述 2022, 47(9): 926-931
Drp1在糖尿病心肌病中的作用机制研究进展
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宋小刚1, 吴冰2, * , 陈永清3, *
作者信息
  • 1兰州大学第二临床医学院，甘肃兰州 730030
  • 2解放军联勤保障部队第940医院老年科，甘肃兰州 730050
  • 3甘肃省中心医院心内科，甘肃兰州 730070

    • 宋小刚，硕士研究生，主要从事糖尿病心肌病发病机制方面的研究

通讯作者:

陈永清，E-mail：;
吴冰，E-mail：
Research progress on the mechanism of Drp1 in diabetic cardiomyopathy
Xiao-Gang Song1, Bing Wu2, * , Yong-Qing Chen3, *
Affiliations
  • 1Second Clinical Medical College of Lanzhou University, Lanzhou, Gansu 730030, China
  • 2Department of Geriatrics, the 940th Hospital of Joint Logistics Support Force of Chinese PLA, Lanzhou, Gansu 730050, China
  • 3Department of Cardiology, Gansu Provincial Central Hospital, Lanzhou, Gansu 730070, China
出版时间: 2022-09-28 doi: 10.11855/j.issn.0577-7402.2022.09.0926
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摘要
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糖尿病心肌病是糖尿病患者严重的慢性不可逆心血管并发症之一。近年来研究发现，线粒体动力学平衡紊乱导致的线粒体功能障碍与糖尿病心肌病的发生密切相关。动力相关蛋白1(Drp1)是线粒体分裂的重要调节因子。研究表明，糖尿病心肌细胞中Drp1活性增强可导致线粒体分裂增加、融合减少，从而引起线粒体功能障碍。Drp1通过诱发心肌细胞氧化应激、能量代谢障碍、细胞凋亡、胰岛素抵抗和脂毒性，导致糖尿病心肌病的发生发展。此外，抑制Drp1的活性可改善糖尿病心肌病的心脏功能。本文对Drp1在糖尿病心肌病中的作用机制进行综述，以期为糖尿病心肌病的防治和药物研发提供新思路。

线粒体分裂  /  动力相关蛋白1  /  糖尿病心肌病  /  心肌细胞  /  损伤机制

Diabetic cardiomyopathy is one of the chronic irreversible and serious cardiovascular complications in diabetic patients. Recent studies have shown that the mitochondrial dysfunction caused by the disturbance of mitochondrial dynamic balance is closely related to the occurrence of diabetic cardiomyopathy. Dynamin related protein 1 (Drp1) is an important regulator of mitochondrial fission. Studies have shown that increased activity of Drp1 in diabetes cardiomyocytes can lead to increased mitochondrial fission and decreased mitochondrial fusion which leads to mitochondrial dysfunction. Drp1 can lead to the occurrence and development of diabetic cardiomyopathy by inducing oxidative stress, energy metabolism disorders, apoptosis,insulin resistance, and lipotoxicity in cardiomyocytes. In addition, inhibition of Drp1 activity may improve cardiac function in diabetic cardiomyopathy. Therefore, the mechanism of Drp1 in diabetic cardiomyopathy have been reviewed in present paper in order to provide new ideas for the prevention and treatment of diabetic cardiomyopathy and drug development.

mitochondrial fission  /  dynamin related protein 1  /  diabetic cardiomyopathy  /  myocardial cell  /  damage mechanism
宋小刚, 吴冰, 陈永清. Drp1在糖尿病心肌病中的作用机制研究进展. 解放军医学杂志, 2022 , 47 (9) : 926 -931 . DOI: 10.11855/j.issn.0577-7402.2022.09.0926
Xiao-Gang Song, Bing Wu, Yong-Qing Chen. Research progress on the mechanism of Drp1 in diabetic cardiomyopathy[J]. Medical Journal of Chinese People’s Liberation Army, 2022 , 47 (9) : 926 -931 . DOI: 10.11855/j.issn.0577-7402.2022.09.0926
正文
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目前，全球糖尿病患者约4.51亿，预计到2045年将增加至6.93亿[1]。超过50%的糖尿病患者死亡或致残的原因为心血管并发症[2]。糖尿病心肌病(diabetic cardiomyopathy，DCM)是一种独立于冠状动脉疾病、高血压和心脏瓣膜病而发生心力衰竭的病理生理状态，早期即可出现心肌纤维化、心肌重塑和舒张功能障碍，随后出现收缩功能障碍，最终发展为心力衰竭[3]。DCM的发生涉及多种机制，包括心脏胰岛素信号传导异常、线粒体功能障碍、氧化应激、炎症反应、钙超载、内质网应激、微血管功能障碍和肾素-血管紧张素-醛固酮系统(RAAS)的激活等[4-5]，其中线粒体功能障碍和氧化应激被认为是DCM发生的主要病理生理机制[6-7]。线粒体是高度动态的细胞器，其分裂与融合平衡失调所致的线粒体功能障碍是许多心血管疾病的始动因素，如内皮功能障碍、心肌肥大、心肌病、心力衰竭、心肌缺血再灌注损伤等[8]。动力相关蛋白1(dynamin related protein 1，Drp1)是线粒体分裂的调节因子，在线粒体功能障碍和线粒体氧化应激中发挥着至关重要的作用。本文围绕Drp1在线粒体分裂及DCM中的作用机制进行综述，旨在为DCM的基础研究和临床诊疗提供新思路。
1 线粒体结构
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线粒体位于细胞质中，由高渗透的外膜和低渗透的内膜组成，膜间隙含有细胞色素C等可溶性酶及半胱氨酸蛋白酶(caspase)-3、caspase-9的前体和辅助因子。内膜的生物氧化过程可产生跨膜电子梯度，并介导电子传输及磷酸化，从而生成三磷酸腺苷(ATP)。基质中包含线粒体脱氧核糖核酸(DNA)、核糖核酸(RNA)、核糖体、酶等(图1A)，是进行三羧酸循环的重要场所。
正常心肌细胞线粒体呈管状、棒状结构，横截面呈椭圆形，长宽比约1.5，密集地排列在心肌纤维间隙中，平均长度约7.97 μm，而过度分裂的线粒体呈碎片状或小而圆形，平均长度约2.83 μm。
2 线粒体的融合与分裂
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线粒体动力学包括线粒体的融合与分裂，线粒体动力蛋白家族均含有三磷酸鸟苷(GTP)酶活性。介导线粒体融合的蛋白有线粒体融合蛋白(Mfn)1、Mfn2及视神经萎缩蛋白1(Opa1)(图1B)。线粒体分裂是一个多步骤的过程，包括线粒体膜的收缩及断裂，这一过程由Drp1及其受体介导，其受体包括线粒体分裂蛋白1(Fis1)、线粒体裂变因子(Mff)、49 kD线粒体动力蛋白(MiD49)和51 kD线粒体动力蛋白(MiD51)(图1C)。线粒体融合与分裂之间的动态平衡不但有利于线粒体的更新及清除，而且在维持心肌细胞收缩功能和能量代谢平衡中也发挥着重要作用[9]。
3 Drp1与线粒体分裂
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Drp1由4个保守区域组成，包括GTP酶结构域、中间结构域、可变结构域和GTP酶效应结构域(GED)。Drp1是一种胞质蛋白，通常以无活性的形式存在于细胞质中。Drp1活化后与Fis1、Mff结合，从胞质转运至线粒体外膜，在膜周围形成环状寡聚体结构，促进线粒体分裂。Drp1与线粒体外膜的结合受多种受体(如Fis1、Mff、MiD49、MiD51等)调节。MiD49及MiD51较Fis1、Mff招募Drp1的能力更强，二者可在无Fis1及Mff协助的情况下将Drp1招募至线粒体外膜，启动分裂。
Drp1的激活和转位受磷酸化、棕榈酰化、泛素化和亚硝酰化的调节，以磷酸化最为重要。Drp1的两个丝氨酸残基(ser616和ser637)通过磷酸化来影响Drp1的活性和定位。Drp1 ser616磷酸化后激活Drp1，使其向线粒体外膜转移，促进线粒体分裂；而Drp1 ser637磷酸化后则可抑制Drp1的活化及Drp1向线粒体外膜的转移，进而抑制线粒体分裂[10-11]。
高血糖、高血脂、缺血缺氧、紫外线辐射等均可使Drp1 ser616磷酸化，促进线粒体分裂。在2型糖尿病(T2DM)中，Drp1、Fis1、Mff的表达水平升高，而Mfn1、Mfn2、OPA1的表达水平明显降低，线粒体分裂增加，线粒体的形态表现为碎片化，且更短更圆。
4 Drp1与DCM
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目前认为，氧化应激、代谢紊乱、心肌纤维化、炎症反应、细胞凋亡、内质网应激等是DCM细胞损伤的主要机制。最新研究发现，Drp1可参与糖尿病心肌细胞的活性氧(ROS)产生、能量代谢异常、糖脂代谢紊乱、胰岛素抵抗及细胞凋亡过程，导致DCM的发生发展，最终进展为心功能不全[12-13]。
4.1 Drp1与氧化应激
烟酰胺腺嘌呤二核苷酸(NADH)和黄素腺嘌呤二核苷酸(FADH2)氧化的电子通过线粒体内膜中的电子传输链(ETC)穿过内膜到达膜间隙，产生电化学梯度，促进无机磷酸与二磷酸腺苷(ADP)结合生成ATP。在糖尿病心肌细胞中，Drp1表达增高，线粒体复合体Ⅰ/Ⅱ/Ⅲ/Ⅳ的功能发生障碍，泛醌自由基延长，从而引起ETC异常电子泄露，并与氧原子结合后导致ROS产生增加[14]。同时，由于胰岛素缺乏或胰岛素抵抗，线粒体代谢底物从葡萄糖转换为脂肪酸，以代偿产生足够的ATP，但这个过程会产生更多的ROS，破坏氧化磷酸化过程[15]。
线粒体是氧化磷酸化的场所，也是ROS的主要来源，低浓度ROS具有细胞内信号转导功能，可发挥信号分子的作用。但高浓度的ROS可诱导细胞应激损伤甚至造成细胞死亡，导致DCM。Drp1过表达或Mfn1敲除后，线粒体分裂增加、融合减少，导致线粒体碎片化，并产生过量的ROS[16]；ROS可增加解偶连蛋白(UCP)的活性，后者可使ATP生成和电子转运分离，导致热量产生增加而ATP生成减少[17]。其次，ROS还可损伤DNA、RNA、脂质、蛋白质及酶，导致糖尿病心肌细胞凋亡增加及DCM的发生。
线粒体不仅是ROS的主要产生部位，也是应激状态下ROS主要的攻击靶点[18]。Drp1过表达产生过量ROS，可导致氧化应激损伤、线粒体膜去极化增加、膜电位下降，并促进线粒体通透转换孔(mPTP)的病理性开放，膜间隙细胞色素C渗漏，进而出现线粒体肿胀、膜破裂及线粒体功能障碍，最终导致心肌细胞死亡[19-20]。氧化应激被认为是糖尿病心肌细胞损伤和DCM发生的罪魁祸首[21-23]。过量的ROS可耗尽细胞内的超氧化物歧化酶[锰超氧化物岐化酶(MnSOD)、铜锌超氧化物岐化酶(CuZnSOD)]和抗氧化酶[过氧化氢酶(CAT)、谷胱甘肽过氧化物酶(GPX)和过氧化物还原酶(PRX)]，导致氧化应激损伤，损害心肌细胞Ca2+泵活性，同时也会降低心肌细胞对Ca2+的敏感性，抑制心肌收缩和舒张功能，从而导致心功能障碍及DCM进展[15, 24]。
4.2 Drp1与能量代谢障碍
心肌细胞能量60%~80%来源于线粒体脂肪酸β-氧化。糖尿病初期，线粒体Drp1表达增高，线粒体分裂增加，葡萄糖氧化磷酸化受损，ATP产生减少，但由于RAAS激活，儿茶酚胺分泌增多，脂肪组织动员加速，血浆游离脂肪酸(FFA)浓度升高，FFA进入心肌细胞增加，脂肪酸β-氧化增强，代偿性产生足够的ATP以维持心肌细胞功能。但随着病情进展，Drp1表达进一步增高，线粒体分裂增加呈碎片状，线粒体复合体Ⅰ/Ⅱ/Ⅲ/Ⅳ的活性明显降低，呼吸链功能受损，线粒体功能障碍，脂肪酸β-氧化能力下降，ATP生成明显减少，导致糖尿病心功能障碍加重。此外，由于ATP合成减少，心肌细胞钙泵功能障碍，导致胞质Ca2+超载，进而损害心肌舒张及收缩功能，加重DCM心功能障碍[21, 25-26]。
4.3 Drp1与细胞凋亡
与健康人相比，糖尿病心肌细胞凋亡增加了85倍，而线粒体功能障碍在糖尿病心肌细胞凋亡中发挥了重要作用[27-28]。DCM的特征是氧化应激和线粒体功能障碍，二者共同导致心肌细胞凋亡增加[29]。糖尿病线粒体Drp1 ser616磷酸化增加，活化的Drp1由胞质向线粒体转移，促进线粒体分裂，进而诱发线粒体内膜mPTP开放、膜电位下降、基质肿胀、线粒体外膜通透性增加，以及细胞色素C被释放至细胞质中，从而使凋亡因子caspase-3、B细胞淋巴瘤2相关X蛋白因子(Bax)活化，启动细胞凋亡程序；同时，ROS产生增加、氧化应激增强，线粒体呼吸链受损、ATP产生减少，内质网应激、炎症细胞因子释放增加，以及RAAS局部激活增加等因素，最终共同导致心肌细胞凋亡增加[30-33]。心肌细胞凋亡增加导致细胞数量减少，心肌收缩功能受损，最终造成心肌重塑、心脏扩大、心功能障碍，导致DCM恶化[34]。
4.4 Drp1与胰岛素抵抗和脂毒性
糖尿病心肌细胞中，Drp1、Fis1表达增多，Mfn1、Mfn2表达减少，线粒体分裂增加，碎片化线粒体增多，管状网络线粒体减少，线粒体动力学失衡。线粒体过度分裂可抑制胰岛素受体底物(IRS1)/蛋白激酶B(Akt)信号通路，并阻止葡萄糖转运体(GLUT)转移至细胞膜转运葡萄糖分子，从而导致胰岛素抵抗。同时，ROS产生增多也可抑制IRS1/Akt信号通路，导致GLUT转运葡萄糖减少，进一步加重胰岛素抵抗。由于胰岛素信号被抑制，GLUT向胞膜募集减少、葡萄糖摄入及氧化磷酸化减少，肌质网钙泵活性下降，心肌细胞内Ca2+浓度升高，导致心肌僵硬，最终发生DCM舒张功能不全[35]。
糖尿病心肌细胞中，由于胰岛素缺乏或胰岛素抵抗，心肌细胞葡萄糖摄取及利用率降低，心肌细胞摄取脂肪酸和β-氧化相对增加，以维持足够的ATP生成[36]。然而，心肌细胞摄取脂肪酸超过了β-氧化的能力，胞质内未完全代谢的脂肪酸增多，从而导致细胞内脂质蓄积和脂毒性增加。其中，二酰甘油(DAG)可通过激活蛋白激酶C(PKC)抑制胰岛素受体，神经酰胺(CER)也可通过抑制Akt而抑制胰岛素信号，诱发胰岛素抵抗。胰岛素抵抗和脂毒性共同导致心肌细胞能量代谢障碍，使心肌肥大、心腔扩大，DCM进一步加重[37-39]。
Drp1转运至线粒体是线粒体分裂的标志，也是发生胰岛素抵抗的必要条件。敲除Drp1或应用Drp1抑制剂阻止Drp1由胞质向线粒体外膜的转运可抑制线粒体分裂、减少线粒体碎片及延长线粒体网络，从而逆转胰岛素抵抗[40]。
5 Drp1抑制剂与DCM
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线粒体分裂抑制剂1(Mdivi-1)可通过减少Drp1 ser616磷酸化来抑制Drp1活化，或通过抑制Drp1的GTP酶活性来抑制Drp1的功能，减少线粒体分裂，从而改善线粒体功能、抑制mPTP开放，减少心肌细胞凋亡。研究发现，Mdivi-1可抑制Drp1活化，使ROS和超氧阴离子产生减少，心肌细胞线粒体复合体Ⅰ/Ⅱ/Ⅲ/Ⅳ的功能改善，线粒体电子传输链ETC活性增强，ATP生成增多，DCM心功能改善[41]。
褪黑素通过SIRT1-PGC1α途径抑制Drp1的表达，并以腺苷酸活化蛋白激酶α(AMPKα)依赖的方式抑制Drp1 ser616的磷酸化，增强Drp1 ser637的磷酸化，从而抑制Drp1的活化、增加Mfn2和Opa1的表达，并可抑制线粒体分裂、增加线粒体融合，抑制mPTP开放、减少细胞色素C释放，减少线粒体膜电位下降及改善线粒体复合体Ⅰ/Ⅱ/Ⅲ/Ⅳ的功能，最终减少心肌细胞凋亡，改善DCM的心功能[42]。
黄芩苷是一种天然的黄酮化合物，可通过减少Drp1 ser616的磷酸化抑制Drp1活化，从而抑制线粒体分裂，并可减轻线粒体肿胀及膜电位下降，抑制心肌细胞凋亡，进而保护心功能，改善DCM的预后[30]。因此，Drp1抑制剂可能成为DCM的一种潜在治疗手段。
6 Drp1敲除的利与弊
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线粒体自噬是清除细胞内异常线粒体的一种防御机制，通过线粒体不对称分裂选择性地清除老化、病理性及受损的线粒体，并通过溶酶体进行降解，是心肌细胞功能自我调节的关键[43-44]。Drp1介导的线粒体分裂与线粒体自噬之间存在相互依赖的关系。Drp1向线粒体募集既是启动分裂的标志，也是启动自噬的关键步骤[11, 45]。DCM中，Drp1 Ser616磷酸化增加，Drp1转移至线粒体增多，同时线粒体自噬也被激活。但是，通过过度下调Drp1的表达来抑制Bnip3诱导的线粒体自噬，可导致细胞内受损线粒体清除减少，反而会加重线粒体功能障碍[46]。
糖尿病心肌细胞中Drp1表达增高，线粒体过度分裂，碎片化的线粒体成为线粒体自噬和溶酶体降解的目标，而有功能的线粒体相对减少，从而导致线粒体功能障碍。但是，过度抑制Drp1的表达也可能导致线粒体自噬被抑制，甚至造成心肌细胞损伤[47]。
研究发现，线粒体分裂是线粒体自噬的先决条件。敲除新生小鼠的Drp1可导致线粒体分裂减少、自噬受损，使受损线粒体蓄积、氧化应激增加、ATP生成减少、钙泵功能障碍，从而使细胞内脂质过氧化物含量升高，细胞电活动受损，以及白细胞介素(IL)-6、肿瘤坏死因子(TNF)-α等炎性因子分泌增加，进而导致严重的肌肉萎缩，危及新生小鼠的心脏发育，最终发生心腔扩张和心力衰竭[48]。
7 总结与展望
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糖尿病心肌细胞中Drp1活化增强，线粒体分裂增加、融合减少，线粒体功能障碍，导致心肌细胞氧化应激增强、能量代谢障碍、细胞凋亡增加、胰岛素抵抗和脂毒性增加，进而诱发糖尿病心肌病的发生发展。抑制Drp1的活化及表达，可减少心肌细胞凋亡，改善DCM心功能，以及延缓病情进展。然而，敲除Drp1后线粒体分裂减少、自噬受损，线粒体功能障碍加重，则可导致心肌细胞受损、心功能障碍加重。因此，线粒体分裂是一把双刃剑，生理性分裂对于线粒体功能至关重要，抑制Drp1的过度活化，保持线粒体分裂与融合之间的动态平衡，才能维持正常的线粒体功能及糖尿病和DCM患者的心脏功能，并改善疾病预后。但是，如何通过Drp1精准平衡线粒体分裂与融合过程，仍需要更多的探索性研究进行验证。
基金
收起
  • 甘肃省自然科学基金(18JR3RA402)
  • 甘肃省卫生健康行业科研计划项目(GSWSKY2020-13)
  • 西北民族大学课题(31920200012)
文献
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参考文献 引证文献
排序方式：
[1]
Cho NH, Shaw JE, Karuranga S, et al. IDF Diabetes Atlas: Global estimates of diabetes prevalence for 2017 and projections for 2045[J]. Diabetes Res Clin Pract, 2018, 138: 271-281.
[2]
Teodoro JS, Nunes S, Rolo AP, et al. Therapeutic options targeting oxidative stress, mitochondrial dysfunction and inflammation to hinder the progression of vascular complications of diabetes[J]. Front Physiol, 2019, 9: 1857.
[3]
Dillmann WH. Diabetic cardiomyopathy[J]. Circ Res, 2019, 124(8): 1160-1162.
[4]
Bhagani H, Nasser SA, Dakroub A, et al. The mitochondria:a target of polyphenols in the treatment of diabetic cardiomyopathy[J]. Int J Mol Sci, 2020, 21(14): 4962.
[5]
Zamora M, Villena JA. Contribution of impaired insulin signaling to the pathogenesis of diabetic cardiomyopathy[J]. Int J Mol Sci, 2019, 20(11): 2833.
[6]
Bai CY, Weng ZY, Xiao C, et al. Research progress on the relationship of mitochondrial dysfunction to diabetic vascular complications[J]. Med J Chin PLA, 2020, 45(3): 323-329.
[白春昀, 翁稚颖, 肖创, 等. 线粒体功能障碍与糖尿病血管并发症关系研究进展[J]. 解放军医学杂志, 2020, 45(3): 323-329.]
[7]
Guo Z, Fan D, Tang QZ. Research progress on the mechanism of action of reactive oxygen species in diabetic cardiomyopathy[J]. Med J Chin PLA, 2020, 45(12): 1294-1298.
[郭振, 樊迪, 唐其柱. 活性氧在糖尿病心肌病中的作用机制研究进展[J]. 解放军医学杂志, 2020, 45(12): 1294-1298.]
[8]
Morales PE, Arias-Durán C, Ávalos-Guajardo Y, et al. Emerging role of mitophagy in cardiovascular physiology and pathology[J]. Mol Aspects Med, 2020, 71: 100822.
[9]
Qiu ZL, Wei Y, Song QQ, et al. The role of myocardial mitochondrial quality control in heart failure[J]. Front Pharmacol, 2019, 10: 1404.
[10]
Adaniya SM, Jin O, Cypress MW, et al. Posttranslational modifications of mitochondrial fission and fusion proteins in cardiac physiology and pathophysiology[J]. Am J Physiol Cell Physiol, 2019, 316(5): C583-C604.
[11]
Tong MM, Zablocki D, Sadoshima J. The role of Drp1 in mitophagy and cell death in the heart[J]. J Mol Cell Cardiol, 2020, 142: 138-145.
[12]
Archer SL. Mitochondrial dynamics-mitochondrial fission and fusion in human diseases[J]. N Engl J Med, 2013, 369(23):2236-2251.
[13]
Lin HY, Weng SW, Chang YH, et al. The causal role of mitochondrial dynamics in regulating insulin resistance in diabetes: link through mitochondrial reactive oxygen species[J]. Oxid Med Cell Longev, 2018, 2018: 7514383.
[14]
Deshpande OA, Mohiuddin SS. Biochemistry, oxidative phosphorylation[M]. StatPearls: StatPearls Publishing, 2021.
[15]
Nguyen BY, Ruiz-Velasco A, Bui T, et al. Mitochondrial function in the heart: the insight into mechanisms and therapeutic potentials[J]. Br J Pharmacol, 2019, 176(22): 4302-4318.
[16]
Sabouny R, Shutt TE. Reciprocal regulation of mitochondrial fission and fusion[J]. Trends Biochem Sci, 2020, 45(7): 564-577.
[17]
Berry BJ, Trewin AJ, Amitrano AM, et al. Use the protonmotive force: mitochondrial uncoupling and reactive oxygen species[J]. J Mol Biol, 2018, 430(21): 3873-3891.
[18]
Ito H, Kurokawa H, Matsui H. Mitochondrial reactive oxygen species and heme, non-heme iron metabolism[J]. Arch Biochem Biophys, 2021, 700: 108695.
[19]
Mushtaq I, Bashir Z, Sarwar M, et al. N-acetyl cysteine, selenium, and ascorbic acid rescue diabetic cardiac hypertrophy via mitochondrial-associated redox regulators[J]. Molecules, 2021, 26(23): 7285.
[20]
Chen X, Liang J, Bin W, et al. Anti-hyperlipidemic, anti-inflammatory, and ameliorative effects of DRP1 inhibition in rats with experimentally induced myocardial infarction[J]. Cardiovasc Toxicol, 2021, 21(12): 1000-1011.
[21]
Mui D, Zhang Y. Mitochondrial scenario: roles of mitochondrial dynamics in acute myocardial ischemia/reperfusion injury[J]. J Recept Signal Transduct Res, 2021, 41(1): 1-5.
[22]
Hu L, Ding MG, Tang DS, et al. Targeting mitochondrial dynamics by regulating Mfn2 for therapeutic intervention in diabetic cardiomyopathy[J]. Theranostics, 2019, 9(13): 3687-3706.
[23]
Checa J, Aran JM. Reactive oxygen species: drivers of physiological and pathological processes[J]. J Inflamm Res, 2020, 13: 1057-1073.
[24]
Goh KY, He L, Song JJ, et al. Mitoquinone ameliorates pressure overload-induced cardiac fibrosis and left ventricular dysfunction in mice[J]. Redox Biol, 2019, 21: 101100.
[25]
Adeva-Andany MM, Carneiro-Freire N, Seco-Filgueira M, et al. Mitochondrial β-oxidation of saturated fatty acids in humans[J]. Mitochondrion, 2019, 46: 73-90.
[26]
Feno S, Butera G, Vecellio Reane D, et al. Crosstalk between calcium and ROS in pathophysiological conditions[J]. Oxid Med Cell Longev, 2019, 2019: 9324018.
[27]
Piao L, Fang YH, Hamanaka RB, et al. Suppression of superoxide-hydrogen peroxide production at site IQ of mitochondrial complex I attenuates myocardial stunning and improves postcardiac arrest outcomes[J]. Crit Care Med, 2020, 48(2):e133-e140.
[28]
Zhou X, Qu YL, Gan GS, et al. Cyclosporine A plus ischemic postconditioning improves neurological function in rats after cardiac resuscitation[J]. Neurocrit Care, 2020, 32(3): 812-821.
[29]
Kakoki M, Bahnson EM, Hagaman JR, et al. Engulfment and cell motility protein 1 potentiates diabetic cardiomyopathy via Rac-dependent and Rac-independent ROS production[J]. JCI Insight, 2019, 4(12): e127660.
[30]
Wu J, Chen H, Qin JH, et al. Baicalin improves cardiac outcome and survival by suppressing Drp1-mediated mitochondrial fission after cardiac arrest-induced myocardial damage[J]. Oxid Med Cell Longev, 2021, 2021: 8865762.
[31]
Kuznetsov AV, Javadov S, Margreiter R, et al. The role of mitochondria in the mechanisms of cardiac ischemia-reperfusion injury[J]. Antioxidants (Basel), 2019, 8(10): 454.
[32]
Šileikytė J, Forte M. The mitochondrial permeability transition in mitochondrial disorders[J]. Oxid Med Cell Longev, 2019, 2019: 3403075.
[33]
Wu W, Liu XX, Han LF. Apoptosis of cardiomyocytes in diabetic cardiomyopathy involves overexpression of glycogen synthase kinase-3β[J]. Biosci Rep, 2019, 39(1): BSR20171307.
[34]
Ramalingam A, Budin SB, Mohd Fauzi N, et al. AngiotensinⅡ type Ⅰ receptor antagonism attenuates nicotine-induced cardiac remodeling, dysfunction, and aggravation of myocardial ischemia-reperfusion injury in rats[J]. Front Pharmacol, 2019, 10: 1493.
[35]
Kaludercic N, di Lisa F. Mitochondrial ROS formation in the pathogenesis of diabetic cardiomyopathy[J]. Front Cardiovasc Med, 2020, 7: 12.
[36]
Lopaschuk GD, Karwi QG, Tian R, et al. Cardiac energy metabolism in heart failure[J]. Circ Res, 2021, 128(10): 1487-1513.
[37]
Chaurasia B, Summers SA. Ceramides in metabolism: key lipotoxic players[J]. Annu Rev Physiol, 2021, 83: 303-330.
[38]
Nakamura M, Sadoshima J. Cardiomyopathy in obesity, insulin resistance and diabetes[J]. J Physiol, 2020, 598(14): 2977-2993.
[39]
Lair B, Laurens C, van den Bosch B, et al. Novel insights and mechanisms of lipotoxicity-driven insulin resistance[J]. Int J Mol Sci, 2020, 21(17): 6358.
[40]
Chang WG, Xiao DD, Ao X, et al. Increased dynamin-related protein 1-dependent mitochondrial fission contributes to high-fat-diet-induced cardiac dysfunction and insulin resistance by elevating tafazzin in mouse hearts[J]. Mol Nutr Food Res, 2019, 63(7): e1801322.
[41]
Maneechote C, Palee S, Kerdphoo S, et al. Pharmacological inhibition of mitochondrial fission attenuates cardiac ischemia-reperfusion injury in pre-diabetic rats[J]. Biochem Pharmacol, 2020, 182: 114295.
[42]
Agil A, Chayah M, Visiedo L, et al. Melatonin improves mitochondrial dynamics and function in the kidney of zücker diabetic fatty rats[J]. J Clin Med, 2020, 9(9): 2916.
[43]
Ma KL, Chen G, Li WH, et al. Mitophagy, mitochondrial homeostasis, and cell fate[J]. Front Cell Dev Biol, 2020, 8: 467.
[44]
Xie D, Li JY, Pei Q, et al. Research advances in the role and mechanism of mitophagy in stem cells[J]. Med J Chin PLA, 2021, 46(11): 1141-1147.
[谢丹, 李婧媛, 裴琴, 等. 线粒体自噬在干细胞中的作用及其机制研究进展[J]. 解放军医学杂志, 2021, 46(11): 1141-1147.]
[45]
Feng ST, Wang ZZ, Yuan YH, et al. Dynamin-related protein 1: a protein critical for mitochondrial fission, mitophagy, and neuronal death in Parkinson's disease[J]. Pharmacol Res, 2020, 151: 104553.
[46]
Wei X, Wu YE, Wang W, et al. Decreased dynamin-related protein 1-related mitophagy induces myocardial apoptosis in the aging heart[J]. Acta Biochim Biophys Sin (Shanghai), 2021, 53(10):1354-1366.
[47]
Catanzaro MP, Weiner A, Kaminaris A, et al. Doxorubicin-induced cardiomyocyte death is mediated by unchecked mitochondrial fission and mitophagy[J]. FASEB J, 2019, 33(10):11096-11108.
[48]
Dulac M, Leduc-Gaudet JP, Reynaud O, et al. Drp1 knockdown induces severe muscle atrophy and remodelling, mitochondrial dysfunction, autophagy impairment and denervation[J]. J Physiol, 2020, 598(17): 3691-3710.
2022年第47卷第9期
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文章信息
doi: 10.11855/j.issn.0577-7402.2022.09.0926
  • 接收时间：2021-11-15
  • 首发时间：2025-12-15
  • 出版时间：2022-09-28
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  • 收稿日期：2021-11-15
  • 录用日期：2021-11-25
基金
Natural Science Foundation of Gansu Province(18JR3RA402)
甘肃省自然科学基金(18JR3RA402)
Scientific Research Project on Health Industry of Gansu Province(GSWSKY2020-13)
甘肃省卫生健康行业科研计划项目(GSWSKY2020-13)
Project of Northwest Minzu University(31920200012)
西北民族大学课题(31920200012)
作者信息
    1兰州大学第二临床医学院，甘肃兰州 730030
    2解放军联勤保障部队第940医院老年科，甘肃兰州 730050
    3甘肃省中心医院心内科，甘肃兰州 730070

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2种不同金属材料的力学参数
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Family		 属数
Number of
genus		 种数
Number of
species		 占总种数比例
Percentage of
total species (%)		 属
Genus		 种数
Number of
species		 占总种数比例
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鹅膏菌科Amanitaceae 2 11 5.26 鹅膏菌属 Amanita 10 4.78
小菇科 Mycenaceae 2 12 5.74 丝盖伞属 Inocybe 5 2.39
多孔菌科 Polyporaceae 8 14 6.70 蜡蘑属 Laccaria 5 2.39
红菇科 Russulaceae 3 23 11.00 小皮伞属 Marasmius 6 2.87
小菇属 Mycena 11 5.26
光柄菇属 Pluteus 5 2.39
红菇属 Russula 17 8.13
栓菌属 Trametes 5 2.39
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