Current progress on the mechanisms of hyperhomocysteinemia-induced vascular injury and use of natural polyphenol compounds

Eur J Pharmacol. 2021 Aug 15:905:174168. doi: 10.1016/j.ejphar.2021.174168. Epub 2021 May 11.

Abstract

Cardiovascular disease is one of the most common diseases in the elderly population, and its incidence has rapidly increased with the prolongation of life expectancy. Hyperhomocysteinemia is an independent risk factor for various cardiovascular diseases, including atherosclerosis, and damage to vascular function plays an initial role in its pathogenesis. This review presents the latest knowledge on the mechanisms of vascular injury caused by hyperhomocysteinemia, including oxidative stress, endoplasmic reticulum stress, protein N-homocysteinization, and epigenetic modification, and discusses the therapeutic targets of natural polyphenols. Studies have shown that natural polyphenols in plants can reduce homocysteine levels and regulate DNA methylation by acting on oxidative stress and endoplasmic reticulum stress-related signaling pathways, thus improving hyperhomocysteinemia-induced vascular injury. Natural polyphenols obtained via daily diet are safer and have more practical significance in the prevention and treatment of chronic diseases than traditional drugs.

Keywords: Atherosclerosis; Endoplasmic reticulum stress; Endothelial dysfunction; Hyperhomocysteinemia; Natural polyphenols; Oxidative stress.

Publication types

  • Review

MeSH terms

  • Animals
  • Biological Products / pharmacology
  • Biological Products / therapeutic use
  • Homocysteine / physiology
  • Humans
  • Hyperhomocysteinemia / complications*
  • Hyperhomocysteinemia / metabolism
  • Polyphenols / pharmacology*
  • Polyphenols / therapeutic use*
  • Protective Agents / pharmacology
  • Protective Agents / therapeutic use
  • Vascular System Injuries / drug therapy*
  • Vascular System Injuries / etiology*
  • Vascular System Injuries / metabolism

Substances

  • Biological Products
  • Polyphenols
  • Protective Agents
  • Homocysteine