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- W3046092593 abstract "Sirtuin-3 (SirT3) and AMPK stimulate mitochondrial biogenesis, which increases mitochondrial turnover and cardiomyocyte regeneration. We studied the effects of SirT3, AMPK, and mitochondrial biogenesis on sepsis-induced myocardial injury. Our data showed that after treating cardiomyocytes with lipopolysaccharide, SirT3 and AMPK levels decreased, and this was followed by mitochondrial dysfunction and cardiomyocyte death. Overexpression of SirT3 activated the AMPK pathway and improved mitochondrial biogenesis, which is required to sustain mitochondrial redox balance, maintain mitochondrial respiration, and suppress mitochondrial apoptosis. Inhibition of mitochondrial biogenesis abolished SirT3/AMPK-induced cardioprotection by causing mitochondrial damage. These findings indicate that SirT3 reduces sepsis-induced myocardial injury by activating AMPK-related mitochondrial biogenesis." @default.
- W3046092593 created "2020-08-03" @default.
- W3046092593 creator A5021936608 @default.
- W3046092593 creator A5048551325 @default.
- W3046092593 date "2020-07-28" @default.
- W3046092593 modified "2023-09-27" @default.
- W3046092593 title "SirT3 activates AMPK-related mitochondrial biogenesis and ameliorates sepsis-induced myocardial injury" @default.
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- W3046092593 doi "https://doi.org/10.18632/aging.103644" @default.
- W3046092593 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/7485737" @default.
- W3046092593 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/32721927" @default.
- W3046092593 hasPublicationYear "2020" @default.
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