{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Peng F"],"funding":["National Natural Science Foundation of China","National Natural Science Foundation of China (National Science Foundation of China)"],"pagination":["133"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11094072"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["9(1)"],"pubmed_abstract":["Sirtuin 3 (SIRT3) is well known as a conserved nicotinamide adenine dinucleotide<sup>+</sup> (NAD<sup>+</sup>)-dependent deacetylase located in the mitochondria that may regulate oxidative stress, catabolism and ATP production. Accumulating evidence has recently revealed that SIRT3 plays its critical roles in cardiac fibrosis, myocardial fibrosis and even heart failure (HF), through its deacetylation modifications. Accordingly, discovery of SIRT3 activators and elucidating their underlying mechanisms of HF should be urgently needed. Herein, we identified a new small-molecule activator of SIRT3 (named 2-APQC) by the structure-based drug designing strategy. 2-APQC was shown to alleviate isoproterenol (ISO)-induced cardiac hypertrophy and myocardial fibrosis in vitro and in vivo rat models. I"],"journal":["Signal transduction and targeted therapy"],"pubmed_title":["2-APQC, a small-molecule activator of Sirtuin-3 (SIRT3), alleviates myocardial hypertrophy and fibrosis by regulating mitochondrial homeostasis."],"pmcid":["PMC11094072"],"funding_grant_id":["22107015","82173666","82073998","82374020"],"pubmed_authors":["Jin W","Zou L","Fan Z","Zhang J","Ouyang L","Liu W","Peng F","Li Z","Han B","Zhu L","Zhao Q","Peng C","Zhan G","Fu L","Chen S","Liao M"],"additional_accession":[]},"is_claimable":false,"name":"2-APQC, a small-molecule activator of Sirtuin-3 (SIRT3), alleviates myocardial hypertrophy and fibrosis by regulating mitochondrial homeostasis.","description":"Sirtuin 3 (SIRT3) is well known as a conserved nicotinamide adenine dinucleotide<sup>+</sup> (NAD<sup>+</sup>)-dependent deacetylase located in the mitochondria that may regulate oxidative stress, catabolism and ATP production. Accumulating evidence has recently revealed that SIRT3 plays its critical roles in cardiac fibrosis, myocardial fibrosis and even heart failure (HF), through its deacetylation modifications. Accordingly, discovery of SIRT3 activators and elucidating their underlying mechanisms of HF should be urgently needed. Herein, we identified a new small-molecule activator of SIRT3 (named 2-APQC) by the structure-based drug designing strategy. 2-APQC was shown to alleviate isoproterenol (ISO)-induced cardiac hypertrophy and myocardial fibrosis in vitro and in vivo rat models. I","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 May","modification":"2026-06-02T06:54:41.125Z","creation":"2026-04-15T03:15:35.522Z"},"accession":"S-EPMC11094072","cross_references":{"pubmed":["38744811"],"doi":["10.1038/s41392-024-01816-1"]}}