Vascular Smooth Muscle Cells in Atherosclerosis
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Discussion
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Implication
Narrative review uncovers multifaceted roles of vascular smooth muscle cell phenotypic switching in atherosclerosis, highlighting novel therapeutic targets for plaque stabilization.
Key Points
- To review the evolving understanding of vascular smooth muscle cell (VSMC) heterogeneity, lineage origins, and phenotypic switching in the progression and stability of atherosclerotic plaques.
- Synthesized findings from recent genetic lineage tracing models evaluating VSMC identity, transdifferentiation, and marker expression.
- Assessed biological drivers across atherogenesis, including embryological origin, phenotypic modulation, cell proliferation, senescence, and apoptosis.
- Genetic lineage tracing reveals that VSMCs undergo extensive phenotypic switching into dedifferentiated states, including macrophage-like cells that lose standard VSMC markers and promote atherosclerosis.
- VSMC proliferation contributes to structural plaque stability across multiple stages of atherogenesis, whereas VSMC senescence and apoptosis exacerbate local vascular inflammation.
Cite This Study
Bennett et al. (2016) studied this question.