Targeting ferroptosis in the maintenance of mitochondrial homeostasis in the realm of septic cardiomyopathy.

Maolong Dong, Jun Ren, Hua Ye, Huantao Hu, Xiaoliang Zhou

Journal: Current opinion in pharmacology 2024;74():102430

PMID: 38237386

Full Text on Elsevier Science View on PubMed

Abstract

Septic cardiomyopathy is one of the predominant culprit factors contributing to the rising mortality in patients with severe sepsis. Among various mechanisms responsible for the etiology of septic heart anomalies, disruption of mitochondrial homeostasis has gained much recent attention, resulting in myocardial inflammation and even cell death. Ferroptosis is a novel category of regulated cell death (RCD) provoked by iron-dependent phospholipid peroxidation through iron-mediated phospholipid (PL) peroxidation, enroute to the rupture of plasma membranes and eventually cell death. This review summarizes the recent progress of ferroptosis in mitochondrial homeostasis during septic cardiomyopathy. We will emphasize the role of mitochondrial iron transport channels and the antioxidant system in ferroptosis. Finally, we will summarize and discuss future research, which should help guide disease treatment.

Address: Department of Burns, Nanfang Hospital, Southern Medical University, Guangzhou, 510515, China; Department of Burns & Plastic and Wound Repair, Ganzhou People's Hospital, Ganzhou, Jiangxi, 341000, China.; Department of Burns, Nanfang Hospital, Southern Medical University, Guangzhou, 510515, China.; Department of Burns & Plastic and Wound Repair, Ganzhou People's Hospital, Ganzhou, Jiangxi, 341000, China.; Department of Burns, Nanfang Hospital, Southern Medical University, Guangzhou, 510515, China. Electronic address: [email protected].; Shanghai Institute of Cardiovascular Diseases, Department of Cardiology, Zhongshan Hospital Fudan University, Shanghai 200032, China; National Clinical Research Center for Interventional Medicine, Shanghai 200032, China. Electronic address: [email protected].

DOI: 10.1016/j.coph.2023.102430

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MeSH Terms: Humans, Ferroptosis, Mitochondria, Cardiomyopathies, Iron, Phospholipids