Mechanism of homocysteine-mediated endothelial injury and its consequences for atherosclerosis

Deqiang Yuan; Jiapeng Chu; Hao Lin; Guoqi Zhu; Jun Qian; Yunan Yu; Tongqing Yao; Fan Ping; Fei Chen; Xuebo Liu

doi:10.3389/fcvm.2022.1109445

Mechanism of homocysteine-mediated endothelial injury and its consequences for atherosclerosis

Front Cardiovasc Med. 2023 Jan 16:9:1109445. doi: 10.3389/fcvm.2022.1109445. eCollection 2022.

Authors

Deqiang Yuan¹, Jiapeng Chu¹, Hao Lin¹, Guoqi Zhu¹, Jun Qian¹, Yunan Yu¹, Tongqing Yao¹, Fan Ping¹, Fei Chen¹, Xuebo Liu¹

Affiliation

¹ Department of Cardiology, Tongji Hospital, School of Medicine, Tongji University, Shanghai, China.

Abstract

Homocysteine (Hcy) is an intermediate amino acid formed during the conversion from methionine to cysteine. When the fasting plasma Hcy level is higher than 15 μmol/L, it is considered as hyperhomocysteinemia (HHcy). The vascular endothelium is an important barrier to vascular homeostasis, and its impairment is the initiation of atherosclerosis (AS). HHcy is an important risk factor for AS, which can promote the development of AS and the occurrence of cardiovascular events, and Hcy damage to the endothelium is considered to play a very important role. However, the mechanism by which Hcy damages the endothelium is still not fully understood. This review summarizes the mechanism of Hcy-induced endothelial injury and the treatment methods to alleviate the Hcy induced endothelial dysfunction, in order to provide new thoughts for the diagnosis and treatment of Hcy-induced endothelial injury and subsequent AS-related diseases.

Keywords: atherosclerosis; endothelial cells; homocysteine; hyperhomocysteinemia; inflammation.

Publication types

Review

Grants and funding

This study was supported by the National Natural Science Foundation of China (Grant Nos. 82170346, 81670403, and 81370390) and Grant of Shanghai Science and Technology Committee (No. 22Y11909800).