<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Van Le TN</submitter><funding>BLRD VA</funding><funding>NHLBI NIH HHS</funding><funding>National Institutes of Health</funding><funding>Florida Department of Health</funding><funding>NIGMS NIH HHS</funding><funding>US Department of Veterans Affairs</funding><pagination>170-180</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9752708</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>637</volume><pubmed_abstract>Sirtuin1 (SIRT1) is involved in regulating substrate metabolism in the cardiovascular system. Metabolic homeostasis plays a critical role in hypertrophic heart failure. We hypothesize that cardiac SIRT1 can modulate substrate metabolism during pressure overload-induced heart failure. The inducible cardiomyocyte Sirt1 knockout (icSirt1&lt;sup>-/-&lt;/sup>) and its wild type littermates (Sirt1&lt;sup>f/f&lt;/sup>) C57BL/6J mice were subjected to transverse aortic constriction (TAC) surgery to induce pressure overload. The pressure overload induces upregulation of cardiac SIRT1 in Sirt1&lt;sup>f/f&lt;/sup> but not icSirt1&lt;sup>-/-&lt;/sup> mice. The cardiac contractile dysfunctions caused by TAC-induced pressure overload occurred in Sirt1&lt;sup>f/f&lt;/sup> but not in icSirt1&lt;sup>-/-&lt;/sup> mice. Intriguingly, Sirt1&lt;sup</pubmed_abstract><journal>Biochemical and biophysical research communications</journal><pubmed_title>Sirtuin 1 aggravates hypertrophic heart failure caused by pressure overload via shifting energy metabolism.</pubmed_title><pmcid>PMC9752708</pmcid><funding_grant_id>R01 HL158515</funding_grant_id><funding_grant_id>R01 GM124108</funding_grant_id><funding_grant_id>I01 BX005625</funding_grant_id><pubmed_authors>Van Le TN</pubmed_authors><pubmed_authors>Li J</pubmed_authors><pubmed_authors>Zoungrana LI</pubmed_authors><pubmed_authors>Fatmi MK</pubmed_authors><pubmed_authors>Wang H</pubmed_authors><pubmed_authors>Ren D</pubmed_authors><pubmed_authors>Krause-Hauch M</pubmed_authors></additional><is_claimable>false</is_claimable><name>Sirtuin 1 aggravates hypertrophic heart failure caused by pressure overload via shifting energy metabolism.</name><description>Sirtuin1 (SIRT1) is involved in regulating substrate metabolism in the cardiovascular system. Metabolic homeostasis plays a critical role in hypertrophic heart failure. We hypothesize that cardiac SIRT1 can modulate substrate metabolism during pressure overload-induced heart failure. The inducible cardiomyocyte Sirt1 knockout (icSirt1&lt;sup>-/-&lt;/sup>) and its wild type littermates (Sirt1&lt;sup>f/f&lt;/sup>) C57BL/6J mice were subjected to transverse aortic constriction (TAC) surgery to induce pressure overload. The pressure overload induces upregulation of cardiac SIRT1 in Sirt1&lt;sup>f/f&lt;/sup> but not icSirt1&lt;sup>-/-&lt;/sup> mice. The cardiac contractile dysfunctions caused by TAC-induced pressure overload occurred in Sirt1&lt;sup>f/f&lt;/sup> but not in icSirt1&lt;sup>-/-&lt;/sup> mice. Intriguingly, Sirt1&lt;sup</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Dec</publication><modification>2025-04-26T07:48:33.216Z</modification><creation>2025-04-06T12:29:50.343Z</creation></dates><accession>S-EPMC9752708</accession><cross_references><pubmed>36403480</pubmed><doi>10.1016/j.bbrc.2022.11.014</doi></cross_references></HashMap>