{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,23]],"date-time":"2026-09-23T04:10:56Z","timestamp":1790136656737,"version":"4.0.1"},"reference-count":31,"publisher":"SAGE Publications","issue":"2","license":[{"start":{"date-parts":[[2010,11,24]],"date-time":"2010-11-24T00:00:00Z","timestamp":1290556800000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["J Cardiovasc Pharmacol Ther"],"published-print":{"date-parts":[[2011,6]]},"abstract":"<jats:p>Background and Objectives: Myocardial hypertrophy is a common clinical finding leading to heart failure and sudden death. Mitofusin 2 (Mfn2), a hyperplasia suppressor protein, is downregulated in hypertrophic heart. This study examined the role of Mfn2 in myocardial hypertrophy and its potential signal pathway. Methods and Results: In in vitro studies, neonatal cardiac myocytes were isolated and cultured. Incubation of cultured cardiomycytes with angiotensin II (Ang II) inhibited gene expression of Mfn2; induced cell hypertrophy and protein synthesis; and activated protein kinase Akt. Pretreatment of cells with AdMfn2\u2014a replication-deficient adenoviral vector encoding rat Mfn2 gene\u2014upregulated Mfn2 expression and subsequently attenuated Ang II-induced cell hypertrophy; protein synthesis; and Akt activation. In in vivo studies, direct gene delivery of AdMfn2 into myocardium decreased the infusion of Ang II-induced atrial natriuretic factor (ANF, a hypertrophic marker) expression and cardiomyocyte cross-sectional area. Consistently, upregulation of Mfn2 in myocardium decreased the thicknesses of anterior and posterior walls of left ventricle (LV) and the ratio of LV mass\/body weight in Ang II-treated rats. Of note, AdGFP (control for AdMfn2) did not affect the effects of Ang II in vitro or in vivo. Conclusions: Upregulation of Mfn2 inhibits Ang II-induced myocardial hypertrophy. In this process, inhibition of Akt activation seems to play a significant role. These findings indicate Mfn2 is a critical protein in modulating myocyte hypertrophy.<\/jats:p>","DOI":"10.1177\/1074248410385683","type":"journal-article","created":{"date-parts":[[2010,11,24]],"date-time":"2010-11-24T22:37:27Z","timestamp":1290638247000},"page":"205-211","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":60,"title":["Mitofusin 2 Inhibits Angiotensin II-Induced Myocardial Hypertrophy"],"prefix":"10.1177","volume":"16","author":[{"given":"Haiyi","family":"Yu","sequence":"first","affiliation":[{"name":"Department of Cardiology, Peking University Third Hospital and Key Laboratory of Molecular Cardiovascular Sciences Ministry of Education, Beijing, PR China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yanhong","family":"Guo","sequence":"additional","affiliation":[{"name":"Department of Cardiology, Peking University Third Hospital and Key Laboratory of Molecular Cardiovascular Sciences Ministry of Education, Beijing, PR China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lin","family":"Mi","sequence":"additional","affiliation":[{"name":"Department of Cardiology, Peking University Third Hospital and Key Laboratory of Molecular Cardiovascular Sciences Ministry of Education, Beijing, PR China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xueying","family":"Wang","sequence":"additional","affiliation":[{"name":"Department of Cardiology, Peking University Third Hospital and Key Laboratory of Molecular Cardiovascular Sciences Ministry of Education, Beijing, PR China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lei","family":"Li","sequence":"additional","affiliation":[{"name":"Department of Cardiology, Peking University Third Hospital and Key Laboratory of Molecular Cardiovascular Sciences Ministry of Education, Beijing, PR China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wei","family":"Gao","sequence":"additional","affiliation":[{"name":"Department of Cardiology, Peking University Third Hospital and Key Laboratory of Molecular Cardiovascular Sciences Ministry of Education, Beijing, PR China,"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"179","published-online":{"date-parts":[[2010,11,24]]},"reference":[{"key":"atypb1","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M809757200"},{"issue":"12","key":"atypb2","doi-asserted-by":"crossref","first-page":"996","DOI":"10.1139\/Y09-105","volume":"87","author":"Espira L.","year":"2009","journal-title":"Can J Physiol Pharmacol."},{"key":"atypb3","doi-asserted-by":"publisher","DOI":"10.1253\/circj.CJ-08-0481"},{"key":"atypb4","doi-asserted-by":"publisher","DOI":"10.1016\/S0008-6363(00)00044-4"},{"key":"atypb5","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.101.10.1130"},{"key":"atypb6","doi-asserted-by":"publisher","DOI":"10.1042\/bj3470275"},{"issue":"19","key":"atypb7","first-page":"17190","volume":"278","author":"Bach D.","year":"2003","journal-title":"A novel regulatory mechanism altered in obesity. 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