ArticleProceedings of the National Academy of Sciences of the United States of America2020
Matrix mechanotransduction mediated by thrombospondin-1/integrin/YAP in the vascular remodeling.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 107 papers.
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Who cites it
107 citing papers in PubMed, 171 citations in OpenAlex.
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- Inactivation Rap2a in Endothelial Cell Prevents Pulmonary Fibrosis by Regulating Immune Microenvironment Through MAP4K4-VCAM1 Signaling.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Integrin-Binding Matricellular Protein Fibulin-5 Maintains Epidermal Stem Cell Heterogeneity During Skin Aging.Aging cell · 2026Article
- Negative-Pressure Induces Epithelial-Mesenchymal Transition via Thrombospondin-1 Upregulation in Intact Diabetic Skin.International wound journal · 2026Article
- Surface-Associated Proteins on Extracellular Vesicles Remodel the Tumor Microenvironment by Potentiating TGF-β Signaling in a Contact-Dependent Manner.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
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- Secretory VSMC-derived THBS1 promotes macrophage M1 polarization and inflammation in intracranial aneurysms via the CD47/NF-κB axis.Frontiers in immunology · 2026Article
- The role of thrombospondin-1 in dermatological conditions.Frontiers in medicine · 2026Review
- Article
47 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The extracellular matrix (ECM) initiates mechanical cues that activate intracellular signaling through matrix-cell interactions. In blood vessels, additional mechanical cues derived from the pulsatile blood flow and pressure play a pivotal role in homeostasis and disease development. Currently, the nature of the cues from the ECM and their interaction with the mechanical microenvironment in large blood vessels to maintain the integrity of the vessel wall are not fully understood. Here, we identified the matricellular protein thrombospondin-1 (Thbs1) as an extracellular mediator of matrix mechanotransduction that acts via integrin αvβ1 to establish focal adhesions and promotes nuclear shuttling of Yes-associated protein (YAP) in response to high strain of cyclic stretch. Thbs1-mediated YAP activation depends on the small GTPase Rap2 and Hippo pathway and is not influenced by alteration of actin fibers. Deletion of
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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.