[Research progress on the role and mechanism of endothelial dysfunction in hyperhomocysteine-induced atherosclerosis]

Area of Science:

• Cardiovascular Science
• Molecular Biology
• Pathophysiology

Background:

• Hyperhomocysteinemia (HHcy) is an independent risk factor for cardiovascular diseases.
• The precise molecular mechanisms linking HHcy to vascular pathogenesis remain unclear.
• Endothelial dysfunction is a critical early event in atherosclerosis and HHcy-related vascular diseases.

Approach:

• This review synthesizes current research on the molecular links between HHcy and endothelial dysfunction.
• It specifically examines how HHcy impacts endothelial cells.
• The review highlights the role of endothelial mesenchymal transition in HHcy-induced vascular damage.

Key Points:

• HHcy induces endothelial dysfunction by promoting oxidative stress, inhibiting nitric oxide and hydrogen sulfide pathways.
• HHcy also triggers endothelial mesenchymal transition, activates coagulation, and causes protein N-homocysteination and cellular hypomethylation.
• Endothelial mesenchymal transition is identified as a significant contributor to HHcy-mediated vascular injury.

Conclusions:

• HHcy contributes to vascular disease through multiple detrimental effects on endothelial cells.
• Endothelial mesenchymal transition represents a key mechanism in HHcy-induced vascular damage.
• Understanding these pathways may offer novel therapeutic strategies for HHcy-related vascular conditions.