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Vascular smooth muscle cell proliferation and migration signaling pathways collectively regulate the transition of VSMCs between contractile and synthetic phenotypes, which is crucial for vascular development, tissue repair, and, if dysregulated, leads to pathological vessel remodeling associated with cardiovascular diseases such as atherosclerosis and restenosis. Core mediators include growth factors (e.g., TGF-β signaling via TGFBR1), MAPK family members (especially ERK and p38), splicing factors like SRSF1, and extracellular matrix modulators including MMP2 and MMP9. These pathways can act independently or coordinately to control the cellular migration, cell-cycle progression, and proliferation of VSMCs. Therapeutic targeting typically focuses on key molecules within these pathways rather than the pathway as a whole, in order to modulate abnormal vascular remodeling while preserving physiological repair processes
Inhibition of growth factor-mediated signal transduction (e.g., ERK, p38 MAPK, TGF-β/Smad3) Suppression of matrix metalloproteinases (MMP2, MMP9 inhibition) Modulation of transcription factors (e.g., KLF5, EGR1)
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