Amelioration of myocardial ischemia-reperfusion injury by SIRT4 involves mitochondrial protection and reduced apoptosis

Biochemical and Biophysical Research Communications
Guangwei ZengHaiyan Wang

Abstract

Apoptosis and mitochondria dysfunction are key contributors to myocardial ischemia-reperfusion (MI-R) injury. SIRT4, a mitochondrial-localized sirtuin, controls cellular energy metabolism and stress response, and is abundantly present in the heart, however, its role in MI-R injury is not clear. In the current study, we demonstrate that SIRT4 is downregulated in cardiomyocytes both in vitro and in vivo models after MI-R. Functionally, SIRT4 overexpression decreases myocardial infarct size and serum creatine phosphokinase (CPK) level, and vice versa, SIRT4 depletion by siRNA increases myocardial infarct size and serum CPK level. Furthermore, we show that these protective roles of SIRT4 against MI-R injury are associated with preserved mitochondrial function and reduced myocardial apoptosis. Taken together, our findings indicate that SIRT4 ameliorates MI-R injury through regulating mitochondrial function and apoptosis, and suggest that manipulating SIRT4 may be of clinical benefit in MI-R injury.

Citations

Dec 12, 2019·Canadian Journal of Physiology and Pharmacology·Shi-Jing WangJun Peng
Jan 23, 2019·Frontiers in Endocrinology·Zheying MinYang Yu
Jan 14, 2021·Cardiovascular Toxicology·Ling HeJuxiang Li
May 1, 2021·International Journal of Molecular Sciences·Liangyu HuDeli Zhang
Jun 29, 2021·Pharmacological Research : the Official Journal of the Italian Pharmacological Society·Keyan WangXiaolong Wang
Aug 17, 2021·Frontiers in Cardiovascular Medicine·Wei ZhaoJianhui Rong
Nov 13, 2021·Clinical and Experimental Pharmacology & Physiology·Marwa MedhetEbtehal El-Demerdash

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