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Article(id=1208518757945839769, tenantId=1146029695717560320, journalId=1189873630562394117, issueId=1208518757253779608, articleNumber=null, orderNo=null, doi=10.11855/j.issn.0577-7402.2021.12.11, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=research-article, receivedDate=1615392000000, receivedDateStr=2021-03-11, revisedDate=1627488000000, revisedDateStr=2021-07-29, acceptedDate=null, acceptedDateStr=null, onlineDate=1766062925084, onlineDateStr=2025-12-18, pubDate=1640620800000, pubDateStr=2021-12-28, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1766062925084, onlineIssueDateStr=2025-12-18, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1766062925084, creator=13701087609, updateTime=1766062925084, updator=13701087609, issue=Issue{id=1208518757253779608, tenantId=1146029695717560320, journalId=1189873630562394117, year='2021', volume='46', issue='12', pageStart='1167', pageEnd='1267', issueExtLink='null', onlineDate='null', pubDate='null', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=0, createTime=1766062924920, creator=13701087609, updateTime=1766062998332, updator=13701087609, preIssue=null, nextIssue=null, ext={EN=IssueExt(id=1208519065233125464, tenantId=1146029695717560320, journalId=1189873630562394117, issueId=1208518757253779608, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1208519065233125465, tenantId=1146029695717560320, journalId=1189873630562394117, issueId=1208518757253779608, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null}, startPage=1239, endPage=1244, ext={EN=ArticleExt(id=1208518758247829660, articleId=1208518757945839769, tenantId=1146029695717560320, journalId=1189873630562394117, language=EN, title=Research progress on the role and mechanism of AMPK in myocardial fibrosis-related diseases, columnId=1190243275882729994, journalTitle=Medical Journal of Chinese People’s Liberation Army, columnName=Review, runingTitle=null, highlight=null, articleAbstract=

Myocardial fibrosis is a common pathological process from various cardiovascular diseases to heart failure, and multiple signal pathways are jointly involved in the development and progression of myocardial fibrosis. AMP-activated protein kinase (AMPK) is a trimer complex widely distributed in human body, which is a central regulator of energy homeostasis involving the regulation of various metabolic responses and signaling pathways in vivo. AMPK interacts with the network of signal pathways related to myocardial fibrosis and jointly mediates the complex pathophysiological changes of myocardial fibrosis. Intervention of AMPK signal pathway provides a new therapeutic idea for the prevention and treatment of myocardial fibrosis. This paper summarizes the role and possible mechanisms of AMPK in different diseases related to cardiac fibrosis. The mutual effects of AMPK in several signaling pathways is also discussed; then further talks about the potential correlations between three kinds of commonly used clinical drugs and AMPK aiming to provide a new idea for the clinical treatment of myocardial fibrosis.

, correspAuthors=Qi-Zhu Tang, authorNote=null, correspAuthorsNote=
*E-mail:
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心肌纤维化是各种心血管疾病进展至心力衰竭的共同病理过程，多条信号通路共同参与了心肌纤维化的发生发展。腺苷酸活化蛋白激酶(AMPK)是一种在人体内广泛分布的三聚体复合物，被称为能量开关，涉及体内多种代谢反应的调控及信号通路的调节。AMPK与心肌纤维化相关信号通路网络相互影响，共同介导了心肌纤维化复杂的病理生理过程。干预AMPK信号通路为心肌纤维化的防治提供了一个新的思路。该文综述了AMPK在多种心肌纤维化相关疾病中的作用及可能机制，进一步探讨了其与几种信号通路的相互影响，并针对三种临床常用药物与AMPK的可能关系进行讨论，旨在加深对AMPK在心肌纤维化中作用的认识及其应用于临床治疗的可能性。

, correspAuthors=唐其柱, authorNote=null, correspAuthorsNote=
唐其柱，E-mail：
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李晨霏，医学硕士，主要从事心力衰竭与心肌重构方面的研究

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李晨霏，医学硕士，主要从事心力衰竭与心肌重构方面的研究

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李晨霏，医学硕士，主要从事心力衰竭与心肌重构方面的研究

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AMPK在心肌纤维化相关疾病中的作用及机制研究进展
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李晨霏 , 樊迪 , 杨政 , 唐其柱 *
解放军医学杂志 | 综述 2021,46(12): 1239-1244
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解放军医学杂志 | 综述 2021, 46(12): 1239-1244
AMPK在心肌纤维化相关疾病中的作用及机制研究进展
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李晨霏, 樊迪, 杨政, 唐其柱*
作者信息
  • 武汉大学人民医院心血管内科/代谢与相关慢病湖北省重点实验室，武汉 430060

    • 李晨霏，医学硕士，主要从事心力衰竭与心肌重构方面的研究

通讯作者:

唐其柱，E-mail：
Research progress on the role and mechanism of AMPK in myocardial fibrosis-related diseases
Chen-Fei Li, Di Fan, Zheng Yang, Qi-Zhu Tang*
Affiliations
  • Department of Cardiology, Renmin Hospital of Wuhan University/Hubei Key Laboratory of Metabolic and Chronic Diseases, Wuhan 430060, China
出版时间: 2021-12-28 doi: 10.11855/j.issn.0577-7402.2021.12.11
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摘要
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心肌纤维化是各种心血管疾病进展至心力衰竭的共同病理过程，多条信号通路共同参与了心肌纤维化的发生发展。腺苷酸活化蛋白激酶(AMPK)是一种在人体内广泛分布的三聚体复合物，被称为能量开关，涉及体内多种代谢反应的调控及信号通路的调节。AMPK与心肌纤维化相关信号通路网络相互影响，共同介导了心肌纤维化复杂的病理生理过程。干预AMPK信号通路为心肌纤维化的防治提供了一个新的思路。该文综述了AMPK在多种心肌纤维化相关疾病中的作用及可能机制，进一步探讨了其与几种信号通路的相互影响，并针对三种临床常用药物与AMPK的可能关系进行讨论，旨在加深对AMPK在心肌纤维化中作用的认识及其应用于临床治疗的可能性。

心肌纤维化  /  腺苷酸活化蛋白激酶  /  信号通路  /  药物治疗

Myocardial fibrosis is a common pathological process from various cardiovascular diseases to heart failure, and multiple signal pathways are jointly involved in the development and progression of myocardial fibrosis. AMP-activated protein kinase (AMPK) is a trimer complex widely distributed in human body, which is a central regulator of energy homeostasis involving the regulation of various metabolic responses and signaling pathways in vivo. AMPK interacts with the network of signal pathways related to myocardial fibrosis and jointly mediates the complex pathophysiological changes of myocardial fibrosis. Intervention of AMPK signal pathway provides a new therapeutic idea for the prevention and treatment of myocardial fibrosis. This paper summarizes the role and possible mechanisms of AMPK in different diseases related to cardiac fibrosis. The mutual effects of AMPK in several signaling pathways is also discussed; then further talks about the potential correlations between three kinds of commonly used clinical drugs and AMPK aiming to provide a new idea for the clinical treatment of myocardial fibrosis.

myocardial fibrosis  /  AMP-activated protein kinase  /  signaling pathway  /  drug treatment
李晨霏, 樊迪, 杨政, 唐其柱. AMPK在心肌纤维化相关疾病中的作用及机制研究进展. 解放军医学杂志, 2021 , 46 (12) : 1239 -1244 . DOI: 10.11855/j.issn.0577-7402.2021.12.11
Chen-Fei Li, Di Fan, Zheng Yang, Qi-Zhu Tang. Research progress on the role and mechanism of AMPK in myocardial fibrosis-related diseases[J]. Medical Journal of Chinese People’s Liberation Army, 2021 , 46 (12) : 1239 -1244 . DOI: 10.11855/j.issn.0577-7402.2021.12.11
正文
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心肌纤维化指细胞外基质生成与降解失衡，间质胶原生成过多且分布异常，是多种心血管疾病的共同病理基础，与心肌重构、缺血再灌注等多种病理变化相关[1-2]。临床现有的治疗手段并不能阻断或逆转心肌纤维化的进展。腺苷酸活化蛋白激酶(AMP-activated protein kinase，AMPK)是一种丝氨酸/苏氨酸蛋白激酶，在机体内广泛表达且高度保守，被称为能量代谢的开关，且与多种疾病过程相关[3-4]。目前，AMPK与糖尿病、肥胖、癌症等的关系已被广泛研究。
AMPK是一种三聚体复合物，包括1个催化亚基α和两个调节亚基β、γ，每个亚基均有不同基因编码的亚型，不同亚型的分布具有一定的组织特异性。AMPK在很多生理和病理条件下均可被激活，最常见的方式为变构激活，呈能量相关性，即当细胞内的ATP减少时，AMP随之升高并与AMPK上游位点结合，使AMPK三聚体结构改变，产生激活效应。激活后的AMPK进一步磷酸化下游靶点，直接或间接地调节限速酶、转录因子、生长因子等的活性，进而参与到代谢等生命活动的调控中。越来越多的证据显示，AMPK在心肌纤维化中也扮演了重要角色，AMPK可通过调节细胞自噬、抑制氧化应激、改善内质网应激等多种途径减轻细胞损伤，发挥抗纤维化作用，同时，AMPK还可激活或抑制其他信号分子，起到抑制肌成纤维细胞分化、改善心功能等作用[5-9]，因此，深入研究AMPK在心肌纤维化中的作用就显得非常重要。
近年的研究表明，AMPK也参与了心肌纤维化的发生发展过程[5]，因此，干预AMPK信号通路对心肌纤维化的防治提供了新的思路。本文围绕AMPK在心肌纤维化相关疾病中的作用、与纤维化信号通路的交叉机制及临床药物治疗的研究进展进行综述，旨在为心肌纤维化相关疾病的治疗提供新的思路。
1 AMPK与心肌纤维化疾病模型
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1.1 压力负荷诱导的心力衰竭
在长期应激状态下，心脏各信号通路与基因表达之间的协调变化可维持正常的心脏功能，包括AMPK的激活。在左心室压力过载之前AMPK的短暂激活可减少不良重塑并保留左心室功能[10]。有研究对野生型和AMPK基因敲除型小鼠行主动脉弓缩窄术(TAC)后发现，AMPK缺失小鼠的心脏明显增大，心功能明显受损，提示AMPK可能对压力超载诱导的心肌肥厚具有保护作用[11]。在此过程中，可能还涉及AMPK与其他信号的相互作用，如PKD2L1缺陷可通过抑制AMPK活性，增加p300介导的钠钙交换体1启动子上组蛋白3赖氨酸27的乙酰化，导致NCX1过表达和线粒体Ca2+超载，从而加重病理性心肌肥厚[12]。此外，Alesutan等[13]在对AMPK亚型进行研究时发现，AMPK α2激活后对衰竭心脏具有保护作用，AMPK α2型缺陷小鼠在TAC后表现出能量代谢相关基因表达功能障碍，使心肌重构加剧；而当压力过载后，AMPK活性增强，但主要表现为AMPK α1亚型的表达升高，而非AMPK α2的减少，因此AMPK α1可能在此心脏损伤模型中起着更重要的作用。
1.2 肥厚型心肌病(HCM)
HCM在人群中的患病率约为0.2%，是常见的遗传性心肌病。左室舒张功能障碍是HCM最重要的病理生理改变，可致患者出现活动时胸闷、气促等症状，甚至发生恶性心律失常、猝死等终点事件。有研究发现，AMPK可提高心肌肥厚小鼠的射血分数，降低心肌细胞的蛋白合成率，并提出AMPK激活后可通过SIRT1信号通路来调控心肌能量代谢，进而抑制心肌肥厚[14]。另一项研究表明，SIRT2的表达和活化在心肌肥厚期间降低，而SIRT2缺乏可加重老年小鼠的心肌肥厚，并降低心脏射血分数；进一步研究发现，SIRT2通过去乙酰化激酶LKB1来维持AMPK信号的激活，进而促进SIRT2在心肌细胞肥大过程中的保护作用[15]。AMPK还可通过激活SIRT3抑制氧化应激引起的心肌肥厚，并改善心功能障碍[16]。此外，近年来关于自噬的研究显示，自噬在心肌肥厚中发挥双重作用，适当的自噬是一种适应性的保护反应，而失去平衡后的过度自噬则会产生负面影响，AMPK可通过抑制mTORC1信号通路而增强自噬[6]。但目前尚不明确是否可利用AMPK来调控自噬的平衡。
1.3 缺血性心肌病
在心肌缺血期间，AMPK的激活是一种重要的心肌细胞应激适应性反应，其激活调节涉及多个方面，包括代谢调节、能量稳态和细胞自噬等。当心肌发生缺血时，AMP生成增加，激活AMPK，进而使激活的AMPK通过刺激葡萄糖摄取和无氧糖酵解来促进葡萄糖的利用，这是在无氧条件下产生ATP的唯一途径，通过糖酵解产生的ATP对维持细胞功能和膜离子梯度至关重要。同时，AMPK可诱导心肌细胞自噬，清除损伤的细胞器[17]。在应激情况下，AMPK转运进入细胞核，进而抑制核糖体RNA(rRNA)的转录及核糖体的生物合成，从而改善内质网应激和细胞死亡[7]。还有研究者观察到在氧糖剥夺的情况下，内皮细胞同时发生了细胞凋亡和自噬诱导[8]。因此，尚不清楚当缺血再灌注发生时AMPK介导的细胞自噬是促进还是抑制细胞死亡。到目前为止，AMPK在细胞自噬及凋亡中的矛盾作用已被多次报道与探讨。此外，Quan等[18]发现年龄也是一个影响因素，与青壮年心脏相比，老龄心脏在缺血应激情况下，AMPK激活的保护作用明显受损，可能的原因是Sesn2作为缺血诱导的支架蛋白与AMPK上游激酶LKB1相互作用，进而启动AMPK磷酸化，然而，在衰老过程中LKB1与Sesn2-AMPK复合物的相互作用受损，最终表现出与年龄相关的现象。
有研究发现，当再灌注发生、氧输送恢复时，AMPK会加速脂肪酸氧化，过多的脂肪酸氧化可能会减弱葡萄糖氧化，导致在葡萄糖摄取和糖酵解增加的情况下乳酸产量增加，这在一定程度上增加了细胞内酸中毒的风险，导致有害的钙超载[19]。但现有的研究无法推断是否一定发生钙超载及其严重程度，而更多的观点认为，AMPK在缺血再灌注过程中扮演的角色利大于弊。因此，AMPK在缺血时对心肌的保护作用引起了广泛的关注。近年来，针对这方面的治疗研究正在成为热点。如褪黑素可通过减少线粒体裂变，重新激活SIRT6和AMPK-PGC-1α-AKT信号传导通路，增强线粒体的合成，进而抑制糖尿病心肌病的发展及随后的心肌缺血/再灌注损伤[20]；曲美他嗪可通过将再灌注过程中的脂肪酸氧化转化为葡萄糖氧化，调节底物代谢，从而改变AMP/ATP比值，触发AMPK信号级联，导致缺血再灌注时心肌氧化应激的降低，同样有助于保护心脏免受缺血/再灌注损伤[21]；而鸢尾素可通过AMPK途径减轻糖尿病小鼠心肌缺血/再灌注损伤，改善线粒体功能，抑制线粒体凋亡[9]。
1.4 糖尿病心肌病
心肌纤维化是糖尿病患者发生心肌重构的一个重要标志。糖尿病心肌病是一种病理性描述，最初表现为心脏僵硬、心肌纤维化、心室肥厚和重塑，进一步发展则出现舒张及收缩功能障碍，最终导致心力衰竭的发生[22]。
有研究对糖尿病模型动物心脏进行解剖，并采用非侵入性T1 mapping对糖尿病患者心脏进行检查，均发现了心肌纤维化，提示在人和动物的糖尿病心肌病中，纤维化为共同的病理改变[23]。有研究通过小鼠实验发现，在心脏中AMPK可能是线粒体相关内质网膜(MAM)的主要调节因子，血糖过高会抑制AMPK，启动Fundc1介导的MAM形成、线粒体功能障碍和心肌病变；相反，心肌细胞中持续激活的AMPK可防止高糖诱导的MAM形成、线粒体Ca2+增加和线粒体功能障碍，提示AMPK诱导的Fundc1抑制是治疗糖尿病心肌病的有效靶点[24]。此外，AMPK也参与了其他代谢反应的调节。AMPK激活在哺乳动物心脏脂质代谢的调节中发挥了重要作用。有研究发现，磷酸化AMPK可通过调控限速酶肉碱棕榈酰转移酶Ⅰ(CPTⅠ)，调节脂肪酸进入线粒体进行脂肪酸氧化的步骤[25]。还有研究发现，在高脂饮食喂养的肥胖小鼠模型中，激活AMPK对肥胖和相关代谢功能障碍具有保护作用。脂肪细胞AMPKα的消融则会损害在寒冷和β-肾上腺素能刺激条件下的适应性产热和能量消耗，从而诱导高脂血症的发生，最终导致肥胖和代谢功能障碍[26]。
AMPK正逐渐成为治疗糖尿病心肌病和其他代谢疾病的靶点，为这类疾病的治疗提供了新思路，如部分抗糖尿病药物可通过激活心肌AMPK磷酸化来减轻心肌纤维化。
2 AMPK与纤维化信号通路的交叉作用
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2.1 AMPK与转化生长因子β(TGF-β)
TGF-β作为细胞超家族的一员，广泛分布在人体各组织中。目前已发现5个亚型，其中活性最强、表达最多的是TGF-β1。有研究表明，TGF-β参与了多种纤维化疾病的发生发展，可促进心肌成纤维细胞的生成，是调节心肌纤维化的重要因子之一[27]。
Juban等[28]构建了肌营养不良模型，通过免疫荧光等方法，发现此种环境可刺激促炎性巨噬细胞分泌更多的TGF-β，直接作用于成纤维细胞，进而促进纤维化；而在给予AMPK激动剂处理后，TGF-β表达被抑制，且观察到肌肉坏死和纤维化区域减少，提示在纤维化的肌肉中，AMPK可通过结合蛋白LTBP4而减少LTBP4的生成，而抑制LTBP4则可使TGF-β分泌减少。Pan等[29]用二甲双胍处理气道平滑肌细胞6 h后，通过酶联免疫吸附实验检测出AMPK磷酸化水平明显升高，同时TGF-β诱导的细胞增殖水平降低，进一步沉默AMPKα2后发现，AMPK活性降低，二甲双胍对TGF-β的作用也减弱，提示AMPK参与介导了此反应。接着，Pan等[29]重复上述实验思路，利用蛋白定量的方法分别分析Smad2/3、miR-206、HDAC4、cyclin D1的变化，发现miR-206、HDAC4、cyclin D1蛋白参与了TGF-β诱导的脂肪间充质干细胞增殖，而AMPK参与介导了这一增殖过程，其中，HDAC4磷酸化和活化发挥了较为重要的作用。此外，CTRP6——一种在心肌梗死细胞中表达并可改善心肌梗死后心功能、减轻心肌纤维化的信号分子，被证实是通过AMPK抑制TGF-β诱导的肌成纤维细胞分化及心肌成纤维细胞迁移来实现保护作用的[30]。
2.2 AMPK与SIRT
Sirtuins家族是一类烟酰胺腺嘌呤二核苷酸(NAD)依赖的组蛋白去乙酰化酶，广泛分布在人体各组织中，参与调节细胞能量代谢、细胞凋亡及衰老等多种过程。既往研究发现，Sirt3基因敲除小鼠更易发生心肌纤维化、心肌肥厚及心功能降低，而AMPK可能通过多种途径与Sirt3发生关联，共同作用于心肌纤维化的发生发展[31]。
在以脂多糖(LPS)诱导的脓毒症心肌细胞模型中，通过RNA提取和对TPS、TR90等数据的分析，发现AMPK和Sirt3对LPS引起的心肌收缩舒张功能降低均有逆转效果[31]。为探究二者之间的关联，进一步将AMPK抑制剂CC添加到Sirt3处理的心肌细胞中，并检测线粒体电子传递链复合物和活性氧活性，结果发现线粒体是连接二者作用的关键，即Sirt3可提高线粒体的活性，而这一过程需要AMPK介导，从而发挥心肌保护作用[31]。此外，AMPK/Sirt3信号通路可在多种情况下被激活。Xu等[32]用腹主动脉束带法构建心肌肥厚模型，测定AMPK下游靶点乙酰辅酶A羧化酶(ACC)的磷酸化水平，并通过siRNA转染来抑制Sirt3的表达水平，发现胆碱可激活AMPK/Sirt3信号通路以减轻心肌肥厚和心肌纤维化程度。而在通过腺病毒介导的Mfn2过表达实验中发现，Mfn2可通过增强线粒体自噬与融合、抑制线粒体凋亡来激活AMPK/Sirt3信号通路，进而消除炎症介导的线粒体损伤，在缺血再灌注中发挥心脏保护作用[33]。这些研究提示，上述不同物质对AMPK/Sirt3信号通路的激活，均可对心功能产生保护作用，未来可成为心血管疾病治疗的靶点。
2.3 AMPK与肾素-血管紧张素系统(renin-angiotensin system，RAS)
RAS自发现以来一直是心血管领域最重要的治疗靶点之一，是一类具有极强的缩血管和刺激肾上腺皮质分泌醛固酮等作用的肽类物质，包括肾素、血管紧张素原、血管紧张素转换酶、血管紧张素(Ang)Ⅰ、Ang Ⅱ等。当肾血流量减少时，会使肾素释放增加，进而导致Ang Ⅱ分泌增多，刺激心肌成纤维细胞增殖及胶原蛋白的合成与沉积，诱导心肌纤维化。
Kröller-Schön等[34]用TekCre+或Cadh5Cre+小鼠和α1AMPKflox/flox小鼠培育出血管内皮特异性AMPK缺失的小鼠品系，注射Ang Ⅱ[0.5 mg/(kg.d)，持续7 d]，结果显示，野生型小鼠内皮仅出现轻度功能障碍，而AMPK敲除小鼠的内皮功能障碍明显加重，波谱测定结果提示可能与AMPK缺失引起的主动脉一氧化氮(NO)表达下降、氧化应激增加有关。同时，AMPK缺失小鼠也可通过上调内皮黏附分子来促进炎性细胞向血管壁集中，加重血管壁损害。此外，该研究还着重观察了诱导血红素加氧酶-1(HO-1)的变化，发现其参与了应激反应，可保护细胞免受氧化损伤；在Ang Ⅱ处理后，AMPK敲除小鼠的内皮细胞和主动脉组织中的HO-1诱导几乎被完全钝化。另有研究发现，Ang Ⅱ注射[0.8 μg/(g.d)]14 d后，氧化应激的3个标志物p-eIF2α、XBP1s、KDEL表达水平均明显升高，而二甲双胍可消除Ang Ⅱ引起的氧化应激，这一消除现象更多依赖于AMPKα2，与AMPKα1比较，AMPKα2敲除后的氧化应激反应更明显，且这一过程需要磷酸受钙蛋白(PLB)磷酸化的参与[35]。
3 AMPK与药物治疗
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3.1 二甲双胍
二甲双胍作为治疗2型糖尿病的一线用药，已经得到广泛关注和研究，近年来，部分学者发现了二甲双胍在其他领域的功效，包括本文所探讨的心肌纤维化相关类疾病。二甲双胍于2001年首次被发现可以激动AMPK，由此展开了一系列相关的研究[36]。
对于进行冠状动脉搭桥术的糖尿病初期患者，术后12个月的追踪随访发现，术前曾长期使用二甲双胍的患者较未曾使用的患者心血管不良事件发生率明显降低[37]。在Ang导致的心肌肥厚中，使用二甲双胍可激活AMPK，进而触发Sirt1/eNOS/p53通路，改善线粒体功能障碍[38]。在糖尿病小鼠模型中进行二甲双胍治疗后发现，磷酸化AMPK表达增加，mTOR表达降低，NLRP3通路被抑制，然而在联合使用AMPK抑制剂后，却呈现出相反的结果，同时二甲双胍对心功能的保护作用也消失了，这是由于二甲双胍在糖尿病心肌病中可通过AMPK/mTOR信号通路抑制NLRP3炎性小体，从而减弱NLRP3引起的细胞死亡和纤维化，发挥心功能保护作用[39]。另外，肝细胞核因子4(HNF4)可促进心肌纤维化和TGF-β1的转录，而二甲双胍可激活AMPK进而抑制HNF4的表达，揭示了二甲双胍抗纤维化的新作用机制[40]。但是，目前对于二甲双胍的使用剂量仍然存在争议。有研究发现，药理浓度下二甲双胍可促进线粒体分裂，从而促进线粒体呼吸，此过程是AMPK依赖性的，具有保护作用；而超药理浓度使用时反而会抑制线粒体呼吸，这可能是由于ADP的不足造成的[41]。因此，在使用二甲双胍改善心肌纤维化时，使用的最佳剂量仍需要进一步研究。
3.2 他汀类药物
Mendieta等[42]通过建立3种不同的动物模型发现，静脉注射阿托伐他汀可减少缺血心肌中的细胞凋亡与炎症反应，与对照组比较，中性粒细胞浸润减少50%，同时可使缺血诱导的瘢痕缩小。阿托伐他汀可激活AMPK/mTOR/raptor信号通路，但它并未影响AMPK蛋白和mRNA的总体水平，而是通过改变磷酸化AMPK的比例、激活下游信号通路来发挥作用的。此外，辛伐他汀也可起到同样的心脏保护效果。有研究发现，在TAC诱导大鼠心肌肥厚的实验中，阿托伐他汀可减轻心肌肥厚，其机制在于阿托伐他汀可激活AMPK，进而促进Foxo1激活，抑制miR-143-3p的水平[43]。他汀类药物对心血管系统的多种保护作用使其在临床被广泛应用，然而其不良反应也较大，骨骼肌损伤的案例时有报道。近来有研究发现，通过一些药物(如黄芪甲苷)促进AMPK的磷酸化，可激活过氧化物酶体增殖活化受体γ辅助活化因子1α(PGC-1α)，上调核呼吸因子1(NRF1)的表达，进而促进能量代谢，抑制骨骼肌细胞凋亡，同时也不会影响他汀类药物的疗效[44]。
3.3 水杨酸盐
水杨酸盐是一种植物提取物，在临床上可被阿司匹林等药物代替，阿司匹林在体内会迅速分解为水杨酸盐。有研究发现，阿司匹林对心肌纤维化有抑制作用，可减轻心肌肥厚与心室重塑[45]。Hawley等[46]发现，水杨酸盐可与A-769662(AMPK激活剂)结合于同一位点，引起变构激活并抑制Thr172的去磷酸化，保护AMPK免受蛋白磷酸酶2ca导致的去磷酸化和失活。同时，通过对比不同浓度水杨酸盐中对照组与实验组细胞的磷酸化比例发现，高浓度(>10 mmol/L)水杨酸盐可通过增加AMP和ADP来激活AMPK，这可能与线粒体解偶联相关。另有学者针对上述提到的线粒体途径展开研究，发现水杨酸盐的促质子效应可解释水杨酸盐诱导线粒体解偶联、体内外氧消耗增加及不依赖AMPK β1的效应，同时还发现其对呼吸作用的影响呈剂量依赖性[47]。因此，虽然水杨酸盐可激活AMPK，抑制心肌纤维化，起到保护心脏的作用，但若要达到在体内激活AMPK的效果，阿司匹林的使用量需超出常规剂量[46]，而过量的阿司匹林又可能导致其他方面的不良反应，因此，对于阿司匹林应用于心肌纤维化的治疗，仍需更多研究加以探讨。
4 总结与展望
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综上所述，AMPK作为心肌纤维化机制研究中的热点，在心力衰竭、糖尿病心肌病、HCM、缺血性心肌病的纤维化过程中发挥了重要作用。AMPK通过与TGF-β、Sirt、RAS等信号通路网络交互影响，共同介导心肌纤维化复杂的病理生理过程。目前AMPK在心肌纤维化中的作用仍存在部分争议，如在缺血再灌注时的利弊权衡等。考虑到AMPK不同亚型的组织特异性，需进一步研究不同亚型的作用及不同药物对不同亚型的影响，为阐明AMPK在心肌纤维化中的作用机制提供可靠的理论依据，以期为干预心肌纤维化提供更好、更安全有效的思路。
基金
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  • 国家自然科学基金(81900219)
  • 国家自然科学基金(81530012)
  • 国家自然科学基金(81800216)
文献
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2021年第46卷第12期
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doi: 10.11855/j.issn.0577-7402.2021.12.11
  • 接收时间：2021-03-11
  • 首发时间：2025-12-18
  • 出版时间：2021-12-28
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  • 收稿日期：2021-03-11
  • 修回日期：2021-07-29
基金
National Natural Science Foundation of China(81900219)
国家自然科学基金(81900219)
National Natural Science Foundation of China(81530012)
国家自然科学基金(81530012)
National Natural Science Foundation of China(81800216)
国家自然科学基金(81800216)
作者信息
    武汉大学人民医院心血管内科/代谢与相关慢病湖北省重点实验室，武汉 430060

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2种不同金属材料的力学参数
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Number of
genus		 种数
Number of
species		 占总种数比例
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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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