ArticleJCI insight2021
Integrin α9 regulates smooth muscle cell phenotype switching and vascular remodeling.
Article in JCI insight, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 29 citations in OpenAlex.
- Proteomic profiling of cephalic vein reveals potential biomarkers for arteriovenous fistula neointimal hyperplasia in ESRD patients.Renal failure · 2026Article
- NCOR1 deficiency in mouse smooth muscle attenuates hypertension and vascular remodeling.Communications biology · 2026Article
- Spatially controlled tenascin-C accumulation contributes to inflammatory disease persistence in giant cell aortitis.JCI insight · 2026Article
- The emerging role of integrin signaling in pulmonary vascular disease.American journal of physiology. Lung cellular and molecular physiology · 2026Review
- An Ang-1-releasing self-assembling peptide coating for inflammation modulation and suppression of smooth muscle proliferation.Frontiers in bioengineering and biotechnology · 2026Article
- Integrin α4 and α9 in trabecular meshwork and Schlemm's canal function: emerging regulators of intraocular pressure homeostasis.Frontiers in cell and developmental biology · 2026Review
- TSPAN4 controls vascular smooth muscle cell phenotypic switching and intimal hyperplasia by targeting TPM1-regulated cytoskeletal organization.Clinical science (London, England : 1979) · 2025Article
- Neutrophil Integrin α9 Impairs Efferocytosis and Worsens Long-Term Recovery After Subarachnoid Hemorrhage.Arteriosclerosis, thrombosis, and vascular biology · 2025Article
- Exploring Integrin α5β1 as a Potential Therapeutic Target for Pulmonary Arterial Hypertension: Insights From Comprehensive Multicenter Preclinical Studies.Circulation · 2025Article
- Research Progress of Regulatory Cell Death in Coronary Microembolization.International journal of medical sciences · 2025Review
- Genetic ablation of myeloid integrin α9 attenuates early atherosclerosis.Journal of leukocyte biology · 2024Article
- Roles of Integrin in Cardiovascular Diseases: From Basic Research to Clinical Implications.International journal of molecular sciences · 2024Review
- Article
- Sacubitril/valsartan inhibits the proliferation of vascular smooth muscle cells through notch signaling and ERK1/2 pathway.BMC cardiovascular disorders · 2024Article
- Review
- Interstitial Fluid Shear Stress Induces the Synthetic Phenotype Switching of VSMCs to Release Pro-calcified Extracellular Vesicles via EGFR-MAPK-KLF5 Pathway.International journal of biological sciences · 2024Article
- Extracellular Matrix Remodeling in Vascular Disease: Defining Its Regulators and Pathological Influence.Arteriosclerosis, thrombosis, and vascular biology · 2023Review
- Targeting Neutrophil α9 Improves Functional Outcomes After Stroke in Mice With Obesity-Induced Hyperglycemia.Stroke · 2023Article
- Insights into the toxicological effects of nanomaterials on atherosclerosis: mechanisms involved and influence factors.Journal of nanobiotechnology · 2023Review
- How vascular smooth muscle cell phenotype switching contributes to vascular disease.Cell communication and signaling : CCS · 2022Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Excessive proliferation of vascular smooth muscle cells (SMCs) remains a significant cause of in-stent restenosis. Integrins, which are heterodimeric transmembrane receptors, play a crucial role in SMC biology by binding to the extracellular matrix protein with the actin cytoskeleton within the SMC. Integrin α9 plays an important role in cell motility and autoimmune diseases; however, its role in SMC biology and remodeling remains unclear. Herein, we demonstrate that stimulated human coronary SMCs upregulate α9 expression. Targeting α9 in stimulated human coronary SMCs, using anti-integrin α9 antibody, suppresses synthetic phenotype and inhibits SMC proliferation and migration. To provide definitive evidence, we generated an SMC-specific α9-deficient mouse strain. Genetic ablation of α9 in SMCs suppressed synthetic phenotype and reduced proliferation and migration in vitro. Mechanistically, suppressed synthetic phenotype and reduced proliferation were associated with decreased focal adhesion kinase/steroid receptor coactivator signaling and downstream targets, including phosphorylated ERK, p38 MAPK, glycogen synthase kinase 3β, and nuclear β-catenin, with reduced transcriptional activation of β-catenin target genes. Following vascular injury, SMC-specific α9-deficient mice or wild-type mice treated with murine anti-integrin α9 antibody exhibited reduced injury-induced neointimal hyperplasia at day 28 by limiting SMC migration and proliferation. Our findings suggest that integrin α9 regulates SMC biology, suggesting its potential therapeutic application in vascular remodeling.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.