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Vascular smooth muscle targets encompass a variety of molecular structures present in or on vascular smooth muscle cells that play critical roles in the regulation of vascular tone, structure, and remodeling. These include receptors (e.g., AT1R, endothelin receptors), ion channels (e.g., TRPV4), enzymes (e.g., protein kinase C), transcription factors (e.g., myocardin, IRF7), and scavenger receptors (SR-A, LOX-1, CD36). Alterations in VSMC function—such as increased proliferation, migration, phenotype switching, and apoptosis—are central to numerous cardiovascular diseases including atherosclerosis, hypertension, restenosis, and arterial calcification. Therapeutic agents can target these molecules to inhibit pathological VSMC activity, restore normal vascular function, and prevent disease progression. However, "vascular smooth muscle targets" covers a wide spectrum of molecules, making it necessary to specify the exact target for structured annotation and drug development[1][2][3][4][5][6][7].
Inhibition of VSMC proliferation (e.g., mTOR inhibitors like rapamycin); Modulation of ion channel function to affect contraction (e.g., TRPV4 antagonists); Blockade of receptor-mediated contraction (e.g., AT1R, endothelin receptor antagonists); Regulation of phenotype switching via transcriptional and signaling modulation
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