Biological Characteristics of Cardiolipin in Cardiovascular Diseases
10.13865/j.cnki.cjbmb.2025.03.1325
- VernacularTitle:心磷脂的生物学特征及其在心血管疾病中的作用
- Author:
Hui-Fei ZHANG
1
;
Yue-Hua JIANG
Author Information
1. 山东中医药大学,中医学院,济南 250355
- Publication Type:Journal Article
- Keywords:
cardiolipin(CL);
metabolic processes;
cardiovascular diseases
- From:
Chinese Journal of Biochemistry and Molecular Biology
2025;41(5):678-686
- CountryChina
- Language:Chinese
-
Abstract:
Cardiolipin(CL)is a special type of polyglycerophospholipid,primarily synthesized in the mitochondrial inner membrane and cristae,and serves as a key component for mitochondrial function.It plays an essential role in the cellular membrane,mitochondrial inner membrane and energy metabolism,especially in maintaining the stability of oxidative phosphorylation and the electron transport chain.Ab-normal metabolism of cardiolipin is closely associated with the occurrence of various cardiovascular disea-ses,particularly in genetic disorders such as Barth syndrome(BTHS).Moreover,the role of cardiolipin peroxides in cardiovascular diseases has been increasingly recognized.Studies have shown that cardiolipin peroxidation not only leads to damage of the mitochondrial inner membrane but also promotes the genera-tion of reactive oxygen species(ROS),thereby enhancing oxidative stress within the cell.Abnormal me-tabolism of cardiolipin is also closely related to the pathogenesis of atherosclerosis,diabetic cardiomyopa-thy,hypertension,and other diseases.Regulating cardiolipin metabolism and repairing its functional de-fects may offer potential strategies for treating these diseases.This review discusses the synthesis,degra-dation,and remodeling processes of cardiolipin,and explores its significant role in cardiovascular disea-ses.The synthesis of cardiolipin relies on various enzymes within the mitochondria,while its remodeling involves key enzymes such as phosphatidyltransferases.Abnormal metabolism of cardiolipin,particularly the CL remodeling defects caused by tafazzin gene mutations in BTHS patients,leads to mitochondrial dysfunction,reduced ATP synthesis,increased oxidative stress,and ultimately results in myocardial and other tissue damage.
