کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5963351 | 1576128 | 2016 | 6 صفحه PDF | دانلود رایگان |

- SIRT3 is a potent deacetylase that govern the lysine deacetylation in the mitochondria.
- SIRT3 has a wide range of substrates and exerts important biological functions.
- SIRT3 plays a key role in oxidative stress, I/R injury, metabolic homeostasis and cellular death.
- The effect of SIRT3 on the cardiac system is complex but mostly protective.
- SIRT3 is a promising new therapeutic target for treating cardiovascular diseases.
SIRT3 belongs to a highly conserved protein family of histone deacetylases and it is rich in mitochondria. As acetyl-modification is one of the important post-translational modifications that prevail in the mitochondria, it is not surprising that SIRT3 plays a key regulatory role in this organelle. SIRT3 has a wide range of substrates that are involved in the physiological and pathological processes of oxidative stress, ischemia-reperfusion injury, mitochondrial metabolism homeostasis and cellular death. These pathophysiological processes are considered as the underlying mechanisms of diseases like cardiac hypertrophy, myocardial infarction and heart failure, indicating the potential roles of SIRT3 in cardiovascular diseases. In this review, we will summarize the emerging roles and therapeutic implications of SIRT3 in cardiovascular diseases by providing an update on the latest understanding of its functions.
Journal: International Journal of Cardiology - Volume 220, 1 October 2016, Pages 700-705