ArticleClinical science (London, England : 1979)2025
TSPAN4 controls vascular smooth muscle cell phenotypic switching and intimal hyperplasia by targeting TPM1-regulated cytoskeletal organization.
Article in Clinical science (London, England : 1979), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Vascular Smooth Muscle Cell Plasticity in Atherosclerosis: Mechanisms, Recent Advances, and Therapeutic Implications.Reviews in cardiovascular medicine · 2026Review
- Prenatal acoustic communication triggers adaptive vascular programming in the developing avian brain.The Journal of experimental biology · 2026Article
- Migrasomes program tissue microenvironment: from physiology to oncology, future perspectives in clinical advances.Journal of the National Cancer Center · 2026Review
- Integrating Chinese medicine and intermittent fasting: A promising approach for treating diabetic vascular calcification.Acta pharmaceutica Sinica. B · 2026Article
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17 authors.
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Abstract
Vascular smooth muscle cell (VSMC) phenotypic switching, followed by enhanced proliferation and migration, is a key event in the development of intimal hyperplasia in diverse vascular diseases. While tetraspanin 4 (TSPAN4) is known to be expressed in the vasculature, its function in VSMC phenotypic switching and vascular disease is currently unknown. Here, we investigated the role of TSPAN4 using an in vitro model of platelet-derived growth factor BB (PDGF-BB)-induced phenotypic switching and an in vivo carotid artery ligation model in wildtype and TSPAN4-deficient mice. Our experiments, including EdU assays, Transwell assays, western blot analysis, and immunoprecipitation, revealed that TSPAN4 expression is elevated in human atherosclerotic arteries, ligated mouse carotid arteries, and PDGF-BB-stimulated VSMCs. Additionally, TSPAN4 overexpression promoted the switch from a contractile to a synthetic phenotype, accompanied by enhanced VSMC proliferation and migration. Conversely, TSPAN4 knockdown inhibited these effects, suppressing PDGF-BB-induced phenotypic switching. Mechanistically, TSPAN4 was found to interact with and influence the expression and localization of tropomyosin-1 (TPM1). This, in turn, affected cytoskeletal organization, ultimately driving phenotypic switching and functional alterations in VSMCs. Finally, we demonstrated that TSPAN4 deficiency in mice attenuated vascular neointimal formation following carotid artery ligation. These findings suggested that TSPAN4 is a promising novel therapeutic target for vascular remodeling and proliferative vascular diseases.
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