期刊
CELLS
卷 11, 期 9, 页码 -出版社
MDPI
DOI: 10.3390/cells11091399
关键词
ferroptosis; heart; iron; myocardial infarction; LV remodeling; heart failure; inflammation
类别
资金
- Hawaii Community Foundation [19ADVC-95461]
- NIH [P20GM113134]
Ferroptosis is an iron-dependent form of regulated cell death characterized by dysfunction of the GPX4 antioxidant system. Inhibiting ferroptosis restores cardiac function and provides protection against I/R injury.
Ferroptosis is an iron-dependent form of regulated cell death and is distinct from other conventional forms of regulated cell death. It is often characterized by the dysfunction of the antioxidant selenoprotein glutathione peroxidase 4 (GPX4) antioxidant system. This loss of antioxidant capacity leads to the peroxidation of lipids and subsequent compromised plasma membrane structure. Disruption of the GPX4 antioxidant system has been associated with various conditions such as cardiomyopathy and ischemia-reperfusion (I/R) injury. GPX4 regulates lipid peroxidation, and chemical or genetic inhibition of GPX4 leads to reduced cardiac function. Iron chelators or antioxidants can be used for inhibiting ferroptosis, which restores functionality in in vivo and ex vivo experiments and confers overall cardioprotective effects against I/R injury. Moreover, suppression of ferroptosis also suppresses inflammation and limits the extent of left ventricle remodeling after I/R injury. Future research is necessary to understand the role of ferroptosis following an ischemic incident and can lead to the discovery of more potential therapeutics that prevent ferroptosis in the heart.
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