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Published on: November 10, 2017

Direct effect of statins on homocysteine-induced endothelial adhesiveness: potential impact to human atherosclerosis

C P Lin1, Y H Chen, W T Lin

  • 1Institute of Public Health, National Yang-Ming University, Taipei, Taiwan.

European Journal of Clinical Investigation
|January 30, 2008
PubMed

Insights

Homocysteine (HCY) increases cardiovascular disease risk by activating endothelial cells. Statins directly inhibit this HCY-induced adhesion by reducing VCAM-1, offering a potential treatment for HCY-related atherosclerosis.

Area of Science:

  • Cardiovascular Research
  • Endothelial Biology
  • Pharmacology

Background:

  • Homocysteine (HCY) is a known risk factor for cardiovascular diseases (CVDs).
  • Previous clinical trials reducing plasma HCY have shown limited benefits.
  • Statins, as 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors, present an alternative therapeutic strategy.

Purpose of the Study:

  • To investigate the effects of HCY on endothelial adhesiveness with mononuclear cells (MNCs) in coronary artery disease (CAD) patients.
  • To examine the direct endothelial protective effects of statins against HCY-induced damage.

Main Methods:

  • MNCs were isolated from CAD patients and healthy subjects.
  • Superoxide production, endothelial adhesiveness, and expression of VCAM-1 and ICAM-1 were analyzed.
  • The impact of HCY stimulation and statin treatment on these parameters was assessed.

Main Results:

  • CAD patients exhibited increased MNC superoxide production, plasma HCY, and CRP levels.
  • HCY significantly enhanced endothelial adhesiveness to MNCs from CAD patients and U937 cells, upregulating VCAM-1 expression.
  • Simvastatin and pravastatin markedly reduced HCY-induced VCAM-1 expression and endothelial-MNC adhesion.

Conclusions:

  • Activated MNCs in CAD patients are crucial for HCY-induced endothelial adhesiveness.
  • Statins offer direct protection by inhibiting HCY-induced endothelial-MNC adhesion through VCAM-1 suppression.
  • This mechanism suggests a potential therapeutic role for statins in HCY-related atherosclerosis.
Abstract

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