ArticleScience advances2024
Cellular stiffness sensing through talin 1 in tissue mechanical homeostasis.
Article in Science advances, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Statistical models to characterize colon tumor stiffness heterogeneity through representative atomic force microscopy maps.Scientific reports · 2026Article
- Cytoskeletal prestress homeostasis is a biological principle that governs living cell structure and function.Mechanobiology in medicine · 2026Review
- Soft tissue mechanosensing and remodeling: the core regulatory role of Piezo/TRPV4 ion channels.Frontiers in cell and developmental biology · 2026Review
- Unlocking the therapeutic potential of cellular mechanobiology.Science advances · 2025Review
- Review
- Mechanically tunable fiber-based hydrogel activates PIEZO1-integrin axis for enhanced bone repair.Journal of nanobiotechnology · 2025Article
- Mathematical modelling of mechanotransduction via RhoA signalling pathways.PLoS computational biology · 2025Article
- DNA-Based Molecular Clamp for Probing Protein Interactions and Structure under Force.ACS nano · 2024Article
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18 authors.
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Abstract
Tissue mechanical properties are determined mainly by the extracellular matrix (ECM) and actively maintained by resident cells. Despite its broad importance to biology and medicine, tissue mechanical homeostasis remains poorly understood. To explore cell-mediated control of tissue stiffness, we developed mutations in the mechanosensitive protein talin 1 to alter cellular sensing of ECM. Mutation of a mechanosensitive site between talin 1 rod-domain helix bundles R1 and R2 increased cell spreading and tension exertion on compliant substrates. These mutations promote binding of the ARP2/3 complex subunit ARPC5L, which mediates the change in substrate stiffness sensing. Ascending aortas from mice bearing these mutations showed less fibrillar collagen, reduced axial stiffness, and lower rupture pressure. Together, these results demonstrate that cellular stiffness sensing contributes to ECM mechanics, directly supporting the mechanical homeostasis hypothesis and identifying a mechanosensitive interaction within talin that contributes to this mechanism.
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