The Role of Peroxisome Proliferator-Activated Receptor in Mediating Cardioprotection Against Ischemia/Reperfusion Injury

被引:21
|
作者
Zhong, Chong-Bin [1 ]
Chen, Xi [1 ]
Zhou, Xu-Yue [1 ]
Wang, Xian-Bao [2 ]
机构
[1] Southern Med Univ, Clin Inst 2, Guangzhou, Guangdong, Peoples R China
[2] Southern Med Univ, Dept Cardiol, Zhujiang Hosp, 253 Middle Gongye Ave, Guangzhou 510282, Guangdong, Peoples R China
基金
中国国家自然科学基金;
关键词
myocardial ischemia; reperfusion injury; peroxisome proliferator-activated receptor; cardioprotection; mechanisms; ISCHEMIA-REPERFUSION INJURY; MESSENGER-RNA EXPRESSION; CORONARY-ARTERY-DISEASE; PPAR-GAMMA ACTIVATION; DIABETIC FATTY RATS; FACTOR-KAPPA-B; MYOCARDIAL-ISCHEMIA; OXIDATIVE STRESS; INSULIN-RESISTANCE; MICROVASCULAR DYSFUNCTION;
D O I
10.1177/1074248417707049
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Myocardial infarction (MI) is a serious cardiovascular disease resulting in high rates of morbidity and mortality. Although advances have been made in restoring myocardial perfusion in ischemic areas, decreases in cardiomyocyte death and infarct size are still limited, attributing to myocardial ischemia/reperfusion (I/R) injury. It is necessary to develop therapies to restrict myocardial I/R injury and protect cardiomyocytes against further damage after MI. Many studies have suggested that peroxisome proliferator-activated receptor (PPAR), a ligand-inducible nuclear receptor that predominantly regulates glucose and lipid metabolism, is a promising therapeutic target for ameliorating myocardial I/R injury. Thus, this review focuses on the role of PPAR in cardioprotection during myocardial I/R. The cardioprotective effects of PPAR, including attenuating oxidative stress, inhibiting inflammatory responses, improving glucose and lipid metabolism, and antagonizing apoptosis, are described. Additionally, the underlying mechanisms of cardioprotective effects of PPAR, such as regulating the expression of target genes, influencing other transcription factors, and modulating kinase signaling pathways, are further discussed.
引用
收藏
页码:46 / 56
页数:11
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