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Published on: October 12, 2017

Contributions of hyperhomocysteinemia to atherosclerosis: Causal relationship and potential mechanisms

Ji Zhou1, Richard C Austin

  • 1Department of Medicine, McMaster University, Hamilton, ON, Canada.

Biofactors (Oxford, England)
|May 19, 2009
PubMed

Insights

High homocysteine levels (HHcy) accelerate atherosclerosis, a key factor in cardiovascular disease. This review explores cellular mechanisms, including endoplasmic reticulum stress and the unfolded protein response, contributing to HHcy-induced vascular damage.

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Cardiovascular Science

Background:

  • Hyperhomocysteinemia (HHcy) is an independent risk factor for cardiovascular diseases like stroke and ischemic heart disease.
  • HHcy can result from genetic mutations or B vitamin deficiencies affecting homocysteine metabolism.
  • Animal models confirm a causal link between HHcy and accelerated atherosclerosis.

Purpose of the Study:

  • To review the cellular mechanisms underlying HHcy's role in atherosclerosis.
  • To emphasize the contributions of endoplasmic reticulum (ER) stress and the unfolded protein response (UPR) in atherogenesis.
  • To discuss recent clinical trials and new findings in mouse models.

Main Methods:

  • In vivo and in vitro studies examining cellular mechanisms of HHcy.
  • Focus on ER stress and UPR pathways.
  • Analysis of clinical trial data and animal model results.

Main Results:

  • Oxidative stress and inflammation are proposed mechanisms for HHcy's atherogenic effects.
  • HHcy-induced ER stress and UPR are recently identified contributors to atherogenesis.
  • Clinical trials on lowering homocysteine levels provide insights into cardiovascular risk.

Conclusions:

  • HHcy plays a significant role in the development and acceleration of atherosclerosis.
  • ER stress and UPR are critical cellular pathways involved in HHcy-induced atherogenesis.
  • Further research and clinical evaluation are ongoing to manage HHcy-related cardiovascular risks.

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