Why the study?
Atherosclerosis and plaque rupture cause major cardiovascular events, and recent progress indicates that hydrogen sulfide mediates plaque stability through cellular and molecular mechanisms.
This review highlights the protective role of endogenous hydrogen sulfide in mediating plaque stability and its potential molecular mechanisms in atherosclerosis.
Mechanisms of plaque rupture remain incompletely defined; leaves open whether antioxidants meaningfully alter rupture risk.
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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Lin et al. (2022) studied this question.
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