Key result
Peroxisome proliferator-activated receptor γ (PPARγ) is a promising therapeutic target for ameliorating myocardial ischemia/reperfusion injury through multiple cardioprotective mechanisms.
Why the study?
Does targeting PPARγ provide cardioprotection against myocardial ischemia/reperfusion injury?
Does targeting PPARγ provide cardioprotection against myocardial ischemia/reperfusion injury?
This review highlights PPARγ as a promising therapeutic target to restrict myocardial ischemia/reperfusion injury after myocardial infarction.
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 γ (PPARγ), 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 PPARγ in cardioprotection during myocardial I/R. The cardioprotective effects of PPARγ, 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 PPARγ, such as regulating the expression of target genes, influencing other transcription factors, and modulating kinase signaling pathways, are further discussed.
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Zhong et al. (2017) conducted a review in Myocardial ischemia/reperfusion injury. Peroxisome proliferator-activated receptor γ (PPARγ) was evaluated. Peroxisome proliferator-activated receptor γ (PPARγ) is a promising therapeutic target for ameliorating myocardial ischemia/reperfusion injury through multiple cardioprotective mechanisms.
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