ArticleJournal of cell science2024
A microtubule stability switch alters isolated vascular smooth muscle Ca2+ flux in response to matrix rigidity.
Article in Journal of cell science, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
6 citing papers in PubMed.
- Proteomic analysis of plasma and extracellular vesicles from subjects with impaired vascular health.Bioscience reports · 2026Article
- The roles of the microtubule cytoskeletal network in cardiac mechanobiology.Journal of cell science · 2026Review
- EMF-induced mesenchymal stem cell migration is mediated by SOCE-dependent calcium influx and modulated by ROCK signaling.Journal of bioenergetics and biomembranes · 2026Article
- The Mechanosensation-Metabolism-Inflammation Axis: The Central Role of Piezo1 and TRPV4 in Hypertension-Related Atherosclerosis.International journal of general medicine · 2026Review
- Molecular and cellular mechanisms of pentadecanoic acid.World journal of biological chemistry · 2025Review
- Microvascular endothelial cells display organ-specific responses to extracellular matrix stiffness.Current research in physiology · 2025Article
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
During ageing, the extracellular matrix of the aortic wall becomes more rigid. In response, vascular smooth muscle cells (VSMCs) generate enhanced contractile forces. Our previous findings demonstrate that VSMC volume is enhanced in response to increased matrix rigidity, but our understanding of the mechanisms regulating this process remain incomplete. In this study, we show that microtubule stability in VSMCs is reduced in response to enhanced matrix rigidity via Piezo1-mediated Ca2+ influx. Moreover, VSMC volume and Ca2+ flux is regulated by microtubule dynamics; microtubule-stabilising agents reduced both VSMC volume and Ca2+ flux on rigid hydrogels, whereas microtubule-destabilising agents increased VSMC volume and Ca2+ flux on pliable hydrogels. Finally, we show that disruption of the microtubule deacetylase HDAC6 uncoupled these processes and increased α-tubulin acetylation on K40, VSMC volume and Ca2+ flux on pliable hydrogels, but did not alter VSMC microtubule stability. These findings uncover a microtubule stability switch that controls VSMC volume by regulating Ca2+ flux. Taken together, these data demonstrate that manipulation of microtubule stability can modify VSMC response to matrix stiffness.
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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 Socratic graph.