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The Role of Hydrogen Sulfide in Plaque Stability
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.
Abstract:
Atherosclerosis is the greatest contributor to cardiovascular events and is involved in the majority of deaths worldwide. Plaque rapture or erosion precipitates life-threatening thrombi, resulting in the obstruction blood flow to the heart (acute coronary syndrome), brain (ischemic stroke) or low extremities (peripheral vascular diseases). Among these events, major causation dues to the plaque rupture. Although the initiation, procession, and precise time of controlling plaque rupture are unclear, foam cell formation and apoptosis, cell death, extracellular matrix components, protease expression and activity, local inflammation, intraplaque hemorrhage, and calcification contribute to the plaque instability. These alterations tightly associate with the function regulation of intraplaque various cell populations. Hydrogen sulfide (H2S) is gasotransmitter derived from methionine metabolism and exerts a protective role in the genesis of atherosclerosis. Recent progress also showed H2S mediated the plaque stability. In this review, we discuss the progress of endogenous H2S modulation on functions of vascular smooth muscle cells, monocytes/macrophages, and T cells, and the molecular mechanism in plaque stability.
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