Endogenous hydrogen sulfide is involved in the pathogenesis of atherosclerosis

Biochem Biophys Res Commun. 2010 May 28;396(2):182-6. doi: 10.1016/j.bbrc.2010.04.061. Epub 2010 Apr 13.

Abstract

Atherosclerosis is a chronic, complex, and progressive pathological process in large and medium sized arteries. The exact mechanism of this process remains unclear. Hydrogen sulfide (H(2)S), a novel gasotransmitter, was confirmed as playing a major role in the pathogenesis of many cardiovascular diseases. It plays a role in vascular smooth muscle cell (VSMC) proliferation and apoptosis, participates in the progress of hyperhomocysteinemia (HHCY), inhibits atherogenic modification of LDL, interferes with vascular calcification, intervenes with platelet function, and there are interactions between H(2)S and inflammatory processes. The role of H(2)S in atherosclerotic pathogenesis highlights the mysteries of atherosclerosis and inspires the search for innovative therapeutic strategies. Here, we review the studies to date that have considered the role of H(2)S in atherosclerosis.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Atherosclerosis / etiology*
  • Atherosclerosis / metabolism
  • Atherosclerosis / pathology
  • Blood Platelets / physiology
  • Calcinosis / metabolism
  • Cell Proliferation / drug effects
  • Humans
  • Hydrogen Sulfide / metabolism*
  • Hydrogen Sulfide / pharmacology
  • Hyperhomocysteinemia / metabolism
  • Inflammation / etiology
  • Inflammation / metabolism
  • Inflammation / pathology
  • Lipoproteins, LDL / metabolism
  • Muscle, Smooth, Vascular / drug effects
  • Muscle, Smooth, Vascular / metabolism
  • Muscle, Smooth, Vascular / pathology*

Substances

  • Lipoproteins, LDL
  • Hydrogen Sulfide