ArticleNature biomedical engineering2021
A dysfunctional TRPV4-GSK3β pathway prevents osteoarthritic chondrocytes from sensing changes in extracellular matrix viscoelasticity.
Article in Nature biomedical engineering, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers, 1 of them a synthesis that pooled it.
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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.
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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
63 citing papers in PubMed, 1 synthesis or guideline pooled it, 100 citations in OpenAlex.
- Alteration in cartilage matrix stiffness as an indicator and modulator of osteoarthritis.Bioscience reports · 2024Pooled it
- Translating mechanobiology in osteoarthritis to biomaterial-informed therapeutic strategies.Mechanobiology in medicine · 2026Review
- Cartilage Extracellular Matrix Homeostasis in Knee Osteoarthritis: Pathomechanisms and Therapeutic Targeting.Journal of cellular and molecular medicine · 2026Review
- Article
- Transforming destructive mechanical cues into therapeutic power: Activation of PIEZO1 and TRPV4 counteracts mechano-induced damage of cellular junctions in Hailey-Hailey disease.Journal of advanced research · 2026Article
- Rational design of immunological programs for functional regenerative niches.Materials today. Bio · 2026Review
- PF4 drives mechanical overload-induced temporomandibular joint osteoarthritis through TLR2-dependent activation of NF-κB.Journal of translational medicine · 2026Article
- Exercise-primed Trpv4+ progenitors sense mechanical to regulate graded transition in enthesis regeneration.Bone & joint research · 2026Article
- Microscale Mechanical Cues in Hydrogels: Engineering Strategies to Modulate Cell Fates in Three Dimensions.Cell biomaterials · 2026Article
- Abnormal Stress Reduced miR-330 Supplementation Alleviates Osteoarthritis Progression by Suppressing Osteochondral Catabolism.Aging cell · 2026Article
- miR-205a mediated suppression of CDH11 disrupts Wnt/β-catenin signaling and impairs chondrocyte differentiation.Cell death discovery · 2026Article
- Micro-nano integrated platforms for osteoarthritis therapy: From spatial manipulation to cellular reprogramming.Materials today. Bio · 2026Review
- Ciliary IFT88 inhibits intervertebral disc degeneration under excessive mechanical stress by regulating endplate cartilage calcification.Journal of advanced research · 2026Article
- Review
- MicroRNA-mediated mechanotransduction and chondrocyte differentiation in mesenchymal stem cells.Animal cells and systems · 2026Review
- Fire needling as a neuromodulatory interface in osteoarthritis management.Clinical rheumatology · 2026Article
- Three-dimensionally-printed biphasic PCL/Regenerative biomaterials · 2026Article
- TRP Channels from Sensory Coding to Physiology.Metabolites · 2025Review
- The role of non-linear viscoelastic hydrogel mechanics in cell culture and transduction.Materials today. Bio · 2025Review
- Open Challenges and Opportunities in Piezoelectricity for Tissue Regeneration.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
3 more citing papers are in PubMed but not listed here.
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Changes in the composition and viscoelasticity of the extracellular matrix in load-bearing cartilage influence the proliferation and phenotypes of chondrocytes, and are associated with osteoarthritis. However, the underlying molecular mechanism is unknown. Here we show that the viscoelasticity of alginate hydrogels regulates cellular volume in healthy human chondrocytes (with faster stress relaxation allowing cell expansion and slower stress relaxation restricting it) but not in osteoarthritic chondrocytes. Cellular volume regulation in healthy chondrocytes was associated with changes in anabolic gene expression, in the secretion of multiple pro-inflammatory cytokines, and in the modulation of intracellular calcium regulated by the ion-channel protein transient receptor potential cation channel subfamily V member 4 (TRPV4), which controls the phosphorylation of glycogen synthase kinase 3β (GSK3β), an enzyme with pleiotropic effects in osteoarthritis. A dysfunctional TRPV4-GSK3β pathway in osteoarthritic chondrocytes rendered the cells unable to respond to environmental changes in viscoelasticity. Our findings suggest strategies for restoring chondrocyte homeostasis in 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 OpenQuestion graph.