SIRT3
安普克
线粒体生物发生
线粒体
医学
锡尔图因
AMP活化蛋白激酶
生物发生
败血症
化学
细胞生物学
内科学
生物
蛋白激酶A
生物化学
基因
乙酰化
磷酸化
出处
期刊:Aging
[Impact Journals, LLC]
日期:2020-07-28
卷期号:12 (16): 16224-16237
被引量:93
标识
DOI:10.18632/aging.103644
摘要
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.
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