ArticleProceedings of the National Academy of Sciences of the United States of America2023
Mechanoepigenetic regulation of extracellular matrix homeostasis via Yap and Taz.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
52 citing papers in PubMed, 64 citations in OpenAlex.
- Mechano-immunomodulatory biomaterials: From immune mechanosensing to translational design.Bioactive materials · 2026Review
- Nascent Extracellular Matrix Converts Biomaterial Cues into Cell Fate Decisions.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- N-Terminal Basic Helix and S120 Phosphorylation Cooperatively Regulate Nuclear Localization of UBE2A/B in Mechanotransduction.Biology · 2026Article
- Failure of morphogenesis in chronic inflammation-associated early tumourigenesis: Extracellular matrix biomechanics as an integrative layer.Biochemistry and biophysics reports · 2026Review
- Cytoskeletal-nuclear control of alveolar fibroblast identity directs lung regeneration.bioRxiv : the preprint server for biology · 2026Article
- Sustained YAP/TAZ activation promotes aberrant alveolar epithelial cell differentiation and drives persistent fibrotic remodeling.JCI insight · 2026Article
- Targeting YAP: mechanistic breakthroughs and therapeutic prospects in reversing organ fibrosis.Molecular and cellular biochemistry · 2026Review
- Mechanobiology-Driven Metabolic Reprogramming: Integrative Roles of YAP/TAZ Signaling and Extracellular Matrix Dynamics.Cell biology international · 2026Review
- A Circuit of Mechanically Regulated Transcription Factors Balances Regenerative and Fibrotic Memory of Mesenchymal Stromal Cells.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- O-SNAP uncovers nanoscale chromatin remodeling in dedifferentiation and stress responses.Nature communications · 2026Article
- A Conceptual Fascial Memory Reset Hypothesis: Mechanobiological Insights into Stacking Fascia as an Ultrasound-Visible Structural Phenotype and the Potential Role of Fascial Hydrorelease.International journal of molecular sciences · 2026Article
- Expansion Microscopy reveals changes in cellular and extracellular structures between healthy and perturbed tendons.bioRxiv : the preprint server for biology · 2026Article
- Chromatin accessibility regulates age-dependent nuclear mechanotransduction.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Tendon-Targeted Knockout of Collagen XII Disrupts Murine Achilles Tendon Structure, Function, and Gene Expression at Later Stages of Postnatal Development.Annals of biomedical engineering · 2026Article
- Mechanoepigenetics in musculoskeletal disease.Osteoarthritis and cartilage · 2026Review
- Stress fiber traction force reshapes chromatin accessibility and YAP binding to direct diverse transcriptional programs in mesenchymal stem cells.Mechanobiology in medicine · 2026Article
- Matrix Stiffness Governs Fibroblasts' Regulation of Gingival Immune Homeostasis.Advanced materials (Deerfield Beach, Fla.) · 2026Article
- Fibroblast-Targeted Nanodelivery Systems: Mechanisms of Collagen Remodeling Regulation and Novel Strategies for Scar Repair.Pharmaceutics · 2026Review
- Mechanobiology of Myelin Generation/Regeneration in Health and Disease.Results and problems in cell differentiation · 2026Review
- Ginsenoside Rg5 mitigates tenocyte deathJournal of ginseng research · 2026Article
Corrections and comments
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
Abstract
Cells integrate mechanical cues to direct fate specification to maintain tissue function and homeostasis. While disruption of these cues is known to lead to aberrant cell behavior and chronic diseases, such as tendinopathies, the underlying mechanisms by which mechanical signals maintain cell function are not well understood. Here, we show using a model of tendon de-tensioning that loss of tensile cues in vivo acutely changes nuclear morphology, positioning, and expression of catabolic gene programs, resulting in subsequent weakening of the tendon. In vitro studies using paired ATAC/RNAseq demonstrate that the loss of cellular tension rapidly reduces chromatin accessibility in the vicinity of Yap/Taz genomic targets while also increasing expression of genes involved in matrix catabolism. Concordantly, the depletion of Yap/Taz elevates matrix catabolic expression. Conversely, overexpression of Yap results in a reduction of chromatin accessibility at matrix catabolic gene loci, while also reducing transcriptional levels. The overexpression of Yap not only prevents the induction of this broad catabolic program following a loss of cellular tension, but also preserves the underlying chromatin state from force-induced alterations. Taken together, these results provide novel mechanistic details by which mechanoepigenetic signals regulate tendon cell function through a Yap/Taz axis.
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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.