Quercetin suppresses TGF-β1-induced proliferation and migration of vascular smooth muscle cells via the Smad2/3/MMP-9 signaling axis.

Authors

Zirun Lu, Ming Ma, Lichong Lu, Ke Pan, Zhong Chen, Hailong Cao

Published in

Biochemical and biophysical research communications. Volume 830. Pages 154236. Jul 02, 2026. Epub Jul 02, 2026.

Abstract

Aberrant proliferation and migration of vascular smooth muscle cells (VSMCs) are central to the pathogenesis of occlusive vascular diseases including atherosclerosis and restenosis. Quercetin, a naturally occurring flavonoid with established cardioprotective properties, has been reported to inhibit VSMC dysfunction, yet the underlying molecular mechanisms remain incompletely defined. Here, we demonstrate that quercetin dose-dependently suppresses TGF-β1-induced proliferation and migration of human aortic VSMCs. Mechanistically, quercetin attenuates TGF-β1-mediated phosphorylation of Smad2/3 and markedly reduces expression of matrix metalloproteinase-9 (MMP-9). Using the selective TGF-β type I receptor inhibitor SB431542, we establish that MMP-9 expression in VSMCs is regulated through the canonical Smad2/3 signaling pathway. Rescue experiments with MMP-9 overexpression reversed the anti-proliferative and anti-migratory effects conferred by TGF-β receptor blockade, confirming MMP-9 as an essential downstream effector. These findings delineate the TGF-β1/Smad2/3/MMP-9 signaling axis as a molecular target of quercetin in VSMCs and provide mechanistic rationale for quercetin-based therapeutic strategies in vascular remodeling diseases.

PMID:
42402230
Bibliographic data and abstract were imported from PubMed on 06 Jul 2026.

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