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Folate improves endothelial function in coronary artery disease: an effect mediated by reduction of intracellular

S N Doshi1, I F McDowell, S J Moat

  • 1Department of Pharmacology, Cardiovascular Sciences Research Group, Wales Heart Research Institute, University of Wales College of Medicine, Heath Park, Cardiff, UK.

Arteriosclerosis, Thrombosis, and Vascular Biology
|July 14, 2001
PubMed

Insights

Folic acid improves endothelial function in coronary artery disease (CAD) patients by reducing superoxide, an effect independent of homocysteine reduction. This highlights a novel therapeutic pathway for cardiovascular health.

Area of Science:

  • Cardiovascular Science
  • Nutritional Biochemistry
  • Endothelial Biology

Background:

  • Homocysteine is a known risk factor for coronary artery disease (CAD).
  • Folic acid's role in improving endothelial function in CAD patients is established, but the underlying mechanism remains unclear.
  • Oxidative stress and endothelial dysfunction are key factors in CAD pathogenesis.

Purpose of the Study:

  • To investigate the effects of folic acid on endothelial function, homocysteine levels, and oxidative stress in CAD patients.
  • To examine the acute impact of 5-methyltetrahydrofolate (5-MTHF) on endothelial function and intracellular superoxide production.

Main Methods:

  • A randomized crossover study involving 52 CAD patients receiving folic acid (5 mg daily) for 6 weeks.
  • Assessment of endothelial function using flow-mediated dilatation (FMD).
  • In vitro experiments using cultured endothelial cells to measure intracellular superoxide.

Main Results:

  • Folic acid significantly increased plasma folate, reduced homocysteine by 19%, and improved FMD.
  • Improvements in FMD did not correlate with homocysteine reduction.
  • Acute administration of 5-MTHF improved FMD without affecting homocysteine levels but abolished homocysteine-induced intracellular superoxide.

Conclusions:

  • Folic acid confers beneficial effects on endothelial function in CAD patients, independent of homocysteine reduction.
  • The mechanism may involve the reduction of intracellular endothelial superoxide.
  • 5-MTHF demonstrates a direct role in improving endothelial function and mitigating oxidative stress.

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