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Vascular smooth muscle targets

Molecular classification
G protein-coupled receptors (e.g., angiotensin II type 1 receptor (AT1R), endothelin-1 receptor), Ion channels (e.g., TRPV4 channel), Enzyme (e.g., protein kinase C, phospholipase C), Transcription factor (e.g., myocardin, interferon regulatory factor 7 (IRF7)), Receptor (e.g., scavenger receptors, LDL receptors), Other: guidance molecule receptor families (e.g., Robo receptors for Slit2 ligand)
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Overview

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].

Other names
vascular smooth muscle therapeutic targetsVSMC targets
02

Mechanism of action

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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Biological functions

Regulation of vascular tone/contractionCell proliferationCell migrationApoptosisSignal transductionVascular remodelingInflammationCell differentiation and phenotypic switching
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Disease associations

Cardiovascular disease (hypertension, atherosclerosis, aneurysm, vascular calcification, arterial stiffness)Restenosis (after angioplasty/graft)Vascular injury responseOther: chronic kidney disease (via arterial calcification)
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Safety considerations

Off-target effects and systemic toxicity (e.g., rapamycin toxicity limits systemic use)Accelerated calcification risk (e.g., Daprodustat)Potential impaired vascular healing
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Interacting drugs

Rapamycin (Sirolimus)

4 more in the full profile.

07

Biomarkers

Not typically molecular biomarkers but phenotypic markers such as increased VSMC proliferation, guidance molecule expression (e.g., Slit2 upregulation after injury)Contractile marker expression (e.g., myocardin)VSMC calcification indicators (for arterial calcification in CKD)

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