Research progress on the role and mechanism of endothelial dysfunction in hyperhomocysteine-induced atherosclerosis.
- Author:
Cheng-Yan WU
1
,
2
;
Xu-Lei DUAN
1
,
2
;
Li-Bo WANG
1
,
2
;
Xue-Hui WANG
1
,
3
Author Information
1. Department of Cardiology, The First Affiliated Hospital of Xinxiang Medical University
2. Heart Center of Xinxiang Medical University, Xinxiang 453100, China.
3. Heart Center of Xinxiang Medical University, Xinxiang 453100, China. 121045@xxmu.edu.cn.
- Publication Type:Journal Article
- MeSH:
Humans;
Atherosclerosis;
Cardiovascular Diseases;
Endothelium, Vascular;
Homocysteine/metabolism*;
Hyperhomocysteinemia/complications*;
Oxidative Stress;
Risk Factors
- From:
Acta Physiologica Sinica
2023;75(5):703-713
- CountryChina
- Language:Chinese
-
Abstract:
Hyperhomocysteinemia (HHcy) is considered to be an independent risk factor for cardiovascular diseases, but the molecular mechanisms underlying its pathogenesis are not fully understood. Endothelial dysfunction is a key initiating factor in the pathogenesis of atherosclerosis, which is commonly observed in almost all HHcy-induced vascular diseases. HHcy promotes oxidative stress, inhibits nitric oxide production, suppresses hydrogen sulfide signaling pathway, promotes endothelial mesenchymal transition, activates coagulation pathways, and promotes protein N-homocysteination and cellular hypomethylation, all of which can cause endothelial dysfunction. This article reviews the specific links between HHcy and endothelial dysfunction, and highlights recent evidence that endothelial mesenchymal transition contributes to HHcy-induced vascular damage, with a hope to provide new ideas for the clinical treatment of HHcy-related vascular diseases.
