{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,27]],"date-time":"2026-03-27T09:42:06Z","timestamp":1774604526094,"version":"3.50.1"},"reference-count":34,"publisher":"American Physiological Society","issue":"5","funder":[{"name":"Science and Technology  Department of Jilin Province, International Collaboration Program","award":["20140414012"],"award-info":[{"award-number":["20140414012"]}]},{"DOI":"10.13039\/100000968","name":"American Heart Association (AHA)","doi-asserted-by":"publisher","award":["10GRNT3170012"],"award-info":[{"award-number":["10GRNT3170012"]}],"id":[{"id":"10.13039\/100000968","id-type":"DOI","asserted-by":"publisher"}]},{"name":"Norman Bethune Program of Jilin University","award":["2015221"],"award-info":[{"award-number":["2015221"]}]},{"DOI":"10.13039\/501100010211","name":"Education Department of Jilin Province","doi-asserted-by":"crossref","award":["2015498"],"award-info":[{"award-number":["2015498"]}],"id":[{"id":"10.13039\/501100010211","id-type":"DOI","asserted-by":"crossref"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Heart and Circulatory Physiology"],"published-print":{"date-parts":[[2017,5,1]]},"abstract":"<jats:p> The objectives of the present study were to investigate the effect of ANG-(1\u20137) on the development of cardiac hypertrophy and to identify the intracellular mechanism underlying this action of ANG-(1\u20137). Blood pressure and heart rate were recorded using radiotelemetry before and after chronic subcutaneous infusion of control (PBS), ANG II, ANG-(1\u20137), or ANG II + ANG-(1\u20137) for 4 wk in normotensive rats. Chronic administration of ANG-(1\u20137) did not affect either basal blood pressure or the ANG II-induced elevation in blood pressure. However, ANG-(1\u20137) significantly attenuated ANG II-induced cardiac hypertrophy and perivascular fibrosis in these rats. These effects of ANG-(1\u20137) were confirmed in cultured cardiomyocytes, in which ANG-(1\u20137) significantly attenuated ANG II-induced increases in cell size. This protective effect of ANG-(1\u20137) was significantly attenuated by pretreatment with A779 (a Mas receptor antagonist) or Mito-TEMPO (a mitochondria-targeting superoxide scavenger) as well as blockade of Sirt3 (a deacetylation-acting protein) by viral vector-mediated overexpression of sirtuin (Sirt)3 short hairpin (sh)RNA. Western blot analysis demonstrated that treatment with ANG-(1\u20137) dramatically increased Sirt3 expression. In addition, ANG-(1\u20137) attenuated the ANG II-induced increase in mitochondrial ROS generation, an effect that was abolished by A779 or Sirt3 shRNA. Moreover, ANG-(1\u20137) increased FoxO3a deacetylation and SOD2 expression, and these effects were blocked by Sirt3 shRNA. In summary, the protective effects of ANG-(1\u20137) on ANG II-induced cardiac hypertrophy and increased mitochondrial ROS production are mediated by elevated SOD2 expression via stimulation of Sirt3-dependent deacetylation of FoxO3a in cardiomyocytes. Thus, activation of the ANG-(1\u20137)\/Sirt3 signaling pathway could be a novel therapeutic strategy in the management of cardiac hypertrophy and associated complications. <\/jats:p><jats:p> NEW &amp; NOTEWORTHY Chronic subcutaneous ANG-(1\u20137) has no effect on ANG II-induced elevations in blood pressure but significantly attenuates ANG II-induced cardiac hypertrophy and fibrosis by a mitochondrial ROS-dependent mechanism. This protective effect of ANG-(1\u20137) against the action of ANG II action is mediated by stimulation of sirtuin-3-mediated deacetylation of FoxO3a, which triggers SOD2 expression. <\/jats:p>","DOI":"10.1152\/ajpheart.00768.2016","type":"journal-article","created":{"date-parts":[[2017,4,15]],"date-time":"2017-04-15T00:35:23Z","timestamp":1492216523000},"page":"H980-H991","source":"Crossref","is-referenced-by-count":62,"title":["Angiotensin-(1\u20137) attenuates angiotensin II-induced cardiac hypertrophy via a Sirt3-dependent mechanism"],"prefix":"10.1152","volume":"312","author":[{"given":"Lirong","family":"Guo","sequence":"first","affiliation":[{"name":"Department of Pathophysiology, Basic College of Medical Sciences, Jilin University, Changchun, Jilin, China;"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ankang","family":"Yin","sequence":"additional","affiliation":[{"name":"Yangzhou First People\u2019s Hospital, Yangzhou, Jiangsu, China;"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Qi","family":"Zhang","sequence":"additional","affiliation":[{"name":"Medical Research Center, Shaanxi University of Chinese Medicine, Xianyang, Shaanxi, China; 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