Regulation of Sirtuins in Sepsis-Induced Myocardial Damage: The Underlying Mechanisms for Cardioprotection

被引:6
作者
Pei, Zuowei [1 ,2 ]
Yao, Wei [3 ]
Wang, Shuo [3 ]
Wu, Yaoxin [2 ]
机构
[1] Dalian Univ Technol, Dept Cardiol, Cent Hosp, Dalian 116033, Liaoning, Peoples R China
[2] Dalian Univ Technol, Fac Med, Dalian 116024, Liaoning, Peoples R China
[3] Dalian Univ, Dept Internal Med, Affiliated Zhong Shan Hosp, Dalian 116001, Liaoning, Peoples R China
来源
FRONTIERS IN BIOSCIENCE-LANDMARK | 2024年 / 29卷 / 02期
关键词
sirtuins; sepsis; myocardial damage; mitochondria; inflammation; NF-KAPPA-B; NLRP3; INFLAMMASOME; CYTOKINE PRODUCTION; DYSFUNCTION; DEACETYLASE; ACTIVATION; SIRT2; INHIBITION; RECEPTOR; SHOCK;
D O I
10.31083/j.fbl2902054
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
070307 [化学生物学]; 071010 [生物化学与分子生物学];
摘要
Sepsis is defined as "a life-threatening organ dysfunction caused by a dysregulated host response to infection". Although the treatment of sepsis has evolved rapidly in the last few years, the morbidity and mortality of sepsis in clinical treatment are still climbing. Sirtuins (SIRTs) are a highly conserved family of histone deacetylation involved in energy metabolism. There are many mechanisms of sepsisinduced myocardial damage, and more and more evidence show that SIRTs play a vital role in the occurrence and development of sepsis-induced myocardial damage, including the regulation of sepsis inflammation, oxidative stress and metabolic signals. This review describes our understanding of the molecular mechanisms and pathophysiology of sepsis-induced myocardial damage, with a focus on disrupted SIRTs regulation. In addition, this review also describes the research status of related therapeutic drugs, so as to provide reference for the treatment of sepsis.
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页数:11
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