Article(id=1292135516678410593, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1292135425250976333, articleNumber=null, orderNo=null, doi=10.13699/j.cnki.1001-6821.2026.10.005, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1777996800000, receivedDateStr=2026-05-06, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1785998713893, onlineDateStr=2026-08-06, pubDate=1779897600000, pubDateStr=2026-05-28, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1785998713893, onlineIssueDateStr=2026-08-06, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1785998713893, creator=13701087609, updateTime=1785998713893, updator=13701087609, issue=Issue{id=1292135425250976333, tenantId=1146029695717560320, journalId=1246415772164075586, year='2026', volume='42', issue='10', pageStart='1351', pageEnd='1500', issueExtLink='null', onlineDate='null', pubDate='1779897600000', pubDateStr='2026-05-28', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=null, createTime=1785998692095, creator='13701087609', updateTime=1786014373634, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext={EN=IssueExt(id=1292201198489202995, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1292135425250976333, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1292201198489202996, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1292135425250976333, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null, downloadFileDto=null}, startPage=1378, endPage=1383, ext={EN=ArticleExt(id=1292135516904903010, articleId=1292135516678410593, tenantId=1146029695717560320, journalId=1246415772164075586, language=EN, title=
Mst1 gene knockout combined with
Nrf2 activation improves the progression of type 2 diabetic cardiomyopathy by enhancing autophagy function, columnId=1246531407326105792, journalTitle=Chinese Journal of Clinical Pharmacology, columnName=Clinical and Basic Bridging Research, runingTitle=null, highlight=null, articleAbstract=
Objective To explore the effect of the Mst1/Nrf2 pathway on myocardial autophagy function in type 2 diabetic mice, and to verify whether Mst1 gene knockout and Nrf2 activation can improve diabetic cardiomyopathy (DCM) by regulating autophagy.
Methods The experimental animals were randomly divided into the following 4 groups, with 8 animals in each group: Control group (6 C57BL/6N mice, standard diet), DCM group (6 C57BL/6N mice), DCM+Mst1-/- group (6 Mst1 gene knockout mice), high-sugar and high-fat diet, DCM+Mst1-/-+Nrf2 group (6 diabetic mice with Mst1 gene knockout intervened by Tert-butylhydroquinone(tBHQ)(50 mg/kg/day)(PHR3512, Sigma-Aldrich). Cardiac function was detected by blood pressure, and autophagy was analyzed by Western blot.
Results The 4w systolic blood pressures of the control group, the high glucose control group, the high glucose Mst1 knockout group, and the high glucose Mst1-/-±Nrf2 group were (103.6±1.43), (117.23±9.80), (111±7.43) and (109.21±3.22) mmHg, respectively, and the 8w systolic blood pressures were (99.09±1.46), (135.78±5.98), (123.57±8.90) and (119.97±6.97) mmHg, respectively. the 12w systolic blood pressures were (106.67±2.32), (138.90±2.00), (126.68±2.98) and (120.63±3.12) mmHg, respectively. The diastolic blood pressures at 4w were (79.50±1.12), (99.24±3.89), (85.03±1.89) and (82.90±3.22) mmHg, respectively. The diastolic blood pressures at 8w were (76.35±2.12), (106.78±5.98), (94.80±3.90) and (88.90±2.90) mmHg, respectively. The diastolic blood pressure at 12w were (78.79±1.70), (101.32±2.13), (93.62±3.98) and (89.02±1.92) mmHg, respectively. The 4-week mean arterial pressures were (87.51±0.41), (117.23±9.80), (85.56±1.46) and (83.91±2.23) mmHg, respectively. The 8-week mean arterial pressures were (84.24±2.41), (116.46±5.68), (104.80±3.91) and (98.90±2.90) mmHg, respectively. the 12-week mean arterial pressures were (86.09±1.74), (101.32±2.13), (103.60±3.37) and (99.02±1.55) mmHg, respectively. Compared with the mice in the Control group, the systolic blood pressure, diastolic blood pressure and mean arterial pressure of the mice in the DCM group, DCM+Mst1-/- group and DCM+Mst1-/-+Nrf2 group were significantly increased (P<0.000 01).
Conclusion Improved cardiac diastolic function in mice with Mst1/Nrf2 activation. This effect is achieved by reducing the expression of p62 protein, further emphasizing that the Mst1/Nrf2 axis exerts its protective function by regulating autophagy-related proteins.
, authors=Jun WANG, Guang-wei LI, Wen-si XU, Lu-lu WANG, Bo LI, Xiao-xu REN, authorsList=Jun WANG, Guang-wei LI, Wen-si XU, Lu-lu WANG, Bo LI, Xiao-xu REN, authorCompany=null, correspAuthors=Guang-wei LI, authorNote=null, correspAuthorsNote=null, 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, fund=null), CN=ArticleExt(id=1292135517244641635, articleId=1292135516678410593, tenantId=1146029695717560320, journalId=1246415772164075586, language=CN, title=
Mst1基因敲除结合
Nrf2激活通过增强自噬功能改善2型糖尿病心肌病研究, columnId=1246531407485489349, journalTitle=中国临床药理学杂志, columnName=临床与基础桥接研究, runingTitle=null, highlight=null, articleAbstract=
目的 探讨Mst1/Nrf2通路对2型糖尿病小鼠心肌自噬功能的影响，并验证Mst1基因敲除和Nrf2激活是否能够通过调节自噬改善糖尿病心肌病（DCM）。
方法 将实验动物随机分为以下4组，每组6只：对照组（C57BL/6N小鼠6只，标准饮食）、DCM组（C57BL/6N小鼠6只）、DCM+ Mst1-/-组（Mst1基因敲除小鼠6只，高糖高脂饮食）、DCM+Mst1-/-+Nrf2组[Tert-butylhydroquinone，tBHQ）（50 mg·kg-1·d-1）（PHR3512，Sigma-Aldrich）干预的Mst1基因敲除的糖尿病小鼠6只]。心脏功能通过血压检测，细胞自噬通过Western blot分析。
结果 对照组、高糖对照组、高糖Mst1敲除组、和高糖Mst1-/-+Nrf2组的4 w收缩压分别为（103.6±1.43）、（117.23±9.80）、（111±7.43）和（109.21±3.22）mmHg，8 w收缩压分别为（99.09±1.46）、（135.78±5.98）、（123.57±8.90）和（119.97±6.97）mmHg，12 w收缩压分别为（106.67±2.32）、（138.90±2.00）、（126.68±2.98）和（120.63±3.12）mmHg；4 w舒张压分别为（79.50±1.12）、（99.24±3.89）、（85.03±1.89）和（82.90±3.22）mmHg，8 w舒张压分别为（76.35±2.12）、（106.78±5.98）、（94.80±3.90）和（88.90±2.90）mmHg，12 w舒张压分别为（78.79±1.70）、（101.32±2.13）、（93.62±3.98）和（89.02±1.92）mmHg；4 w平均动脉压分别为（87.51±0.41）、（117.23±9.80）、（85.56±1.46）和（83.91±2.23）mmHg，8 w平均动脉压分别为（84.24±2.41）、（116.46±5.68）、（104.80±3.91）和（98.90±2.90）mmHg，12 w平均动脉压分别为（86.09±1.74）、（101.32±2.13）、（103.60±3.37）和（99.02±1.55）mmHg。与对照组小鼠相比，DCM组小鼠、DCM+Mst1-/-组小鼠和DCM+Mst1-/-+Nrf2组小鼠的收缩压、舒张压以及平均动脉压均明显升高（均P<0.000 01）。
结论 激活Mst1/Nrf2的小鼠改善的心脏舒张功能。这种效应是通过降低p62蛋白的表达来实现的，进一步强调了Mst1/Nrf2轴通过调节自噬相关蛋白来发挥其保护作用。
, authors=王珺, 李光伟, 徐文思, 王璐璐, 李波, 任晓旭, authorsList=王珺, 李光伟, 徐文思, 王璐璐, 李波, 任晓旭, authorCompany=null, correspAuthors=李光伟, authorNote=
王珺（1984-），女，博士，讲师，主要从事糖尿病心肌病的病理生理学研究
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