ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2024
The chondrocyte "mechanome": Activation of the mechanosensitive ion channels TRPV4 and PIEZO1 drives unique transcriptional signatures.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.
What it found
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The trial behind it
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
27 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Standardized Effect Measures Informing Next-Generation Strategies for Mechanical Stimulation in Cartilage Tissue Engineering.Advanced healthcare materials · 2026Pooled it
- Piezo1-mediated Mechanotransduction in the musculoskeletal system: Signaling networks and therapeutic perspectives.Bone reports · 2026Review
- Submolecular modulation of PIEZO1 mechanotransduction with wireless tailor-made nanoswitches.Bioactive materials · 2026Article
- Compressive stress-driven mechanosignaling in chondrocytes: From molecular mechanism to scaffold engineering and translational opportunities.Materials today. Bio · 2026Review
- Article
- PIEZO1 variants that reduce open channel probability are associated with familial osteoarthritis.The Journal of biological chemistry · 2026Article
- MiRNA-Mediated Regulation in Osteoarthritis Across Joint Tissues, Including Translational Perspectives in Dogs.Animals : an open access journal from MDPI · 2026Review
- PIEZO mechanosensitivity in chondrocytes is differentially modulated by L-type and T-type voltage-sensitive ion channels.Osteoarthritis and cartilage open · 2026Article
- A damaging mutation in COL6A3 alters the mechanobiologic response of chondrocytes derived from human induced pluripotent stem cells.Stem cell research & therapy · 2026Article
- Triamcinolone Modulates Chondrocyte Biomechanics and Calcium-Dependent Mechanosensitivity.International journal of molecular sciences · 2026Article
- Exercise-Based Mechanotherapy: From Biomechanical Principles and Mechanotransduction to Precision Regenerative Rehabilitation.International journal of molecular sciences · 2026Review
- From mechanotransduction to manual therapy: advances in piezo/TRP channels and lumbar degeneration.Frontiers in physiology · 2026Review
- From mechanical adaptation to innate immune reprogramming in osteoarthritis: a load-immunity framework.Frontiers in immunology · 2026Review
- Deciphering osteoarthritis cartilage heterogeneity: gene expression-guided patient stratification and microbiome correlations.Frontiers in microbiology · 2026Article
- Ultrasound neuromodulation in brain disorders: from mechanotransduction mechanisms to clinical translation.Frontiers in neuroscience · 2026Review
- Integrating Mechanical Loading, Mechanotransduction, and Biological Responses in Musculoskeletal Tissues Across the Lifespan: Regulation Influenced by Cells, Extracellular Matrix, and Sex.Results and problems in cell differentiation · 2026Review
- Molecular mediators of motion: RNA-RBP networks in exercise-induced osteoarthritis protection.Frontiers in genetics · 2026Review
- The Translational Biology of Temporomandibular Disorder Pain: Mechanisms, Biomarkers, and Therapeutic Perspectives.Journal of pain research · 2026Review
- Pathogenesis of Osteoarthritis: Mechanisms of Action of Disulfidptosis and Targeted Therapeutic Strategies.Drug design, development and therapy · 2026Review
- The Mechanosensation-Metabolism-Inflammation Axis: The Central Role of Piezo1 and TRPV4 in Hypertension-Related Atherosclerosis.International journal of general medicine · 2026Review
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
The mechanosensitive ion channels Transient Receptor Potential Vanilloid 4 (TRPV4) and PIEZO1 transduce physiologic and supraphysiologic magnitudes of mechanical signals in the chondrocyte, respectively. TRPV4 activation promotes chondrogenesis, while PIEZO1 activation by supraphysiologic deformations drives cell death. The mechanisms by which activation of these channels discretely drives changes in gene expression to alter cell behavior remain to be determined. To date, no studies have contrasted the transcriptomic response to activation of these channels nor has any published data attempted to correlate these transcriptomes to alterations in cellular function. This study used RNA sequencing to comprehensively investigate the transcriptomes associated with activation of TRPV4 or PIEZO1, revealing that TRPV4 and PIEZO drive distinct transcriptomes and also exhibit unique co-regulated clusters of genes. Notably, activation of PIEZO1 through supraphysiologic deformation induced a transient inflammatory profile that overlapped with the interleukin (IL)-1-responsive transcriptome and contained genes associated with cartilage degradation and osteoarthritis progression. However, both TRPV4 and PIEZO1 were also shown to elicit anabolic effects. PIEZO1 expression promoted a pro-chondrogenic transcriptome under unloaded conditions, and daily treatment with PIEZO1 agonist Yoda1 significantly increased sulfated glycosaminoglycan deposition in vitro. These findings emphasize the presence of a broad "mechanome" with distinct effects of TRPV4 and PIEZO1 activation in chondrocytes, suggesting complex roles for PIEZO1 in both the physiologic and pathologic responses of chondrocytes. The identification of transcriptomic profiles unique to or shared by PIEZO1 and TRPV4 (distinct from IL-1-induced inflammation) could inform future therapeutic designs targeting these channels for the management and treatment of osteoarthritis.
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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.