Abstract

Sepsis is a serious complication of infection, and its further development may lead to multi-organ dysfunction syndrome. Sepsis cardiomyopathy is a common complication of sepsis and has been directly linked to high mortality. Although the pathogenesis of septic cardiomyopathy is not fully understood, in-depth study of the pathogenesis of septic cardiomyopathy and the identification of its potential therapeutic targets may reduce mortality in patients with sepsis. Ferroptosis is an iron-dependent mode of cell death that has been shown to be involved in the pathophysiological mechanisms of many diseases. Some related studies have reported that ferroptosis may be a potential mechanism of septic cardiomyopathy. This review provides new insights into the mechanisms of mitochondrial dysfunction, lipid peroxidation, xc-system, glutathione peroxidase 4 (GPX4), iron metabolism and the role of ferroptosiswith septic cardiomyopathy for further research and treatment of septic cardiomyopathy.

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