Ferroptosis: a potential new therapeutic target for myocardial injury induced by acute carbon monoxide poisoning.
10.3760/cma.j.cn121430-20241021-00862
- Author:
Anping LIU
1
;
Xuheng JIANG
2
,
3
;
Tianjing SUN
2
,
3
;
Mo LI
2
,
3
;
Haizhen DUAN
2
,
3
;
Shuhong WANG
2
,
3
;
Anyong YU
2
,
3
Author Information
1. Dalian Medical University, Dalian 116044, Liaoning, China.
2. Department of Emergency, Affiliated Hospital of Zunyi Medical University, Zunyi 563003, Guizhou, China. Corresponding author: Yu Anyong, Email: anyongyu@
3. com.
- Publication Type:English Abstract
- MeSH:
Humans;
Carbon Monoxide Poisoning/complications*;
Ferroptosis;
Lipid Peroxidation;
Myocardium/pathology*;
Oxidative Stress
- From:
Chinese Critical Care Medicine
2025;37(4):407-412
- CountryChina
- Language:Chinese
-
Abstract:
Acute carbon monoxide poisoning (ACMP) is one of the most common gas poisonings in the emergency department, with tens of thousands of people seeking medical attention for carbon monoxide (CO) poisoning each year. The severity of poisoning is dependent upon environmental and human factors, with hypoxia and oxidative stress being important mechanisms of cardiac toxicity induced by CO. Myocardial involvement is common in moderate to severe ACMP, including myocardial injury, myocardial infarction, arrhythmia, and sudden death, which are associated with a high risk of death. Ferroptosis is a cell death mechanism caused by iron-dependent lipid peroxidation (LPO), although ferroptosis has been shown to play a critical role in various cardiovascular diseases, the potential mechanism by which it contributes to ACMP-induced myocardial injury is unclear. This review discusses the established link between ferroptosis and cardiovascular disease and summarizes the potential role of ferroptosis in ACMP-induced myocardial injury and the detrimental effects of ACMP on the heart. Elucidating these mechanisms could guide the development of novel therapeutic strategies that target ferroptosis to mitigate ACMP-induced myocardial injury. This review aims to provide a theoretical foundation for future research on the potential use of ferroptosis as a therapeutic target for ACMP-induced myocardial injury.
