The Role of Hydrogen Sulfide in Plaque Stability

Qian Lin1, Bin Geng1

  • 1State Key Laboratory of Cardiovascular Disease, National Center for Cardiovascular Diseases, Fuwai Hospital of Chinese Academy of Medical Sciences, Peking Union Medical College, Beijing 100023, China.

Insights

Hydrogen sulfide (H2S) plays a protective role in atherosclerosis by stabilizing plaques. This review explores how H2S influences key cells and mechanisms involved in plaque stability.

Area of Science:

  • Cardiovascular Research
  • Molecular Biology
  • Pathophysiology

Background:

  • Atherosclerosis is a leading cause of global mortality, driven by plaque rupture leading to thrombotic events.
  • Plaque instability arises from complex factors including foam cell formation, apoptosis, inflammation, and intraplaque hemorrhage.
  • Hydrogen sulfide (H2S), a gasotransmitter, is recognized for its protective effects against atherosclerosis development and progression.

Purpose of the Study:

  • To review the current understanding of endogenous hydrogen sulfide (H2S) in modulating plaque stability.
  • To elucidate the molecular mechanisms by which H2S influences cellular functions within atherosclerotic plaques.
  • To highlight the role of H2S in regulating vascular smooth muscle cells, monocytes/macrophages, and T cells.

Main Methods:

  • Literature review of studies investigating H2S and atherosclerosis.
  • Analysis of research on H2S modulation of cellular functions in plaque development.
  • Examination of molecular pathways involved in H2S-mediated plaque stability.

Main Results:

  • Endogenous H2S exerts protective effects on atherosclerosis genesis.
  • H2S has been shown to mediate and enhance plaque stability.
  • H2S influences the function of key intraplaque cell populations, including vascular smooth muscle cells, monocytes/macrophages, and T cells.

Conclusions:

  • Hydrogen sulfide (H2S) is a critical endogenous modulator of atherosclerotic plaque stability.
  • Understanding H2S's molecular mechanisms offers potential therapeutic strategies for cardiovascular diseases.
  • Targeting H2S pathways may represent a novel approach to prevent or treat atherosclerosis-related events.

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