{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,29]],"date-time":"2026-07-29T13:50:13Z","timestamp":1785333013101,"version":"3.55.0"},"reference-count":48,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal of Applied Physiology"],"published-print":{"date-parts":[[2011,4]]},"abstract":"<jats:p> We reported previously that although there is disruption of coordinated cardiac hypertrophy and angiogenesis in transition to heart failure, matrix metalloproteinase (MMP)-9 induced antiangiogenic factors play a vital role in this process. Previous studies have shown the cardioprotective role of hydrogen sulfide (H<jats:sub>2<\/jats:sub>S) in various cardiac diseases, but its role during transition from compensatory hypertrophy to heart failure is yet to be unveiled. We hypothesize that H<jats:sub>2<\/jats:sub>S induces MMP-2 activation and inhibits MMP-9 activation, thus promoting angiogenesis, and mitigates transition from compensatory cardiac hypertrophy to heart failure. To verify this, aortic banding (AB) was created to mimic pressure overload in wild-type (WT) mice, which were treated with sodium hydrosulfide (NaHS, H<jats:sub>2<\/jats:sub>S donor) in drinking water and compared with untreated control mice. Mice were studied at 3 and 8 wk. In the NaHS-treated AB 8 wk group, the expression of MMP-2, CD31, and VEGF was increased while the expression of MMP-9, endostatin, angiostatin, and tissue inhibitor of matrix metalloproteinase (TIMP)-3 was decreased compared with untreated control mice. There was significant reduction in fibrosis in NaHS-treated groups. Echocardiograph and pressure-volume data revealed improvement of cardiac function in NaHS-treated groups over untreated controls. These results show that H<jats:sub>2<\/jats:sub>S by inducing MMP-2 promotes VEGF synthesis and angiogenesis while it suppresses MMP-9 and TIMP-3 levels, inhibits antiangiogenic factors, reduces intracardiac fibrosis, and mitigates transition from compensatory hypertrophy to heart failure. <\/jats:p>","DOI":"10.1152\/japplphysiol.01064.2010","type":"journal-article","created":{"date-parts":[[2011,1,14]],"date-time":"2011-01-14T06:16:23Z","timestamp":1294985783000},"page":"1093-1100","source":"Crossref","is-referenced-by-count":53,"title":["Hydrogen sulfide mitigates transition from compensatory hypertrophy to heart failure"],"prefix":"10.1152","volume":"110","author":[{"given":"Srikanth","family":"Givvimani","sequence":"first","affiliation":[{"name":"Department of Physiology and Biophysics, University of Louisville School of Medicine, Louisville, 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