ArticleNature communications2021
Neuropathy-causing TRPV4 mutations disrupt TRPV4-RhoA interactions and impair neurite extension.
Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
What it found
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Who cites it
33 citing papers in PubMed, 55 citations in OpenAlex.
- Mechanobiological Response of Osteocyte TRPV4 Base on the Piezoelectricity of Bone Matrix.Annals of biomedical engineering · 2026Article
- Taxane-induced conformational changes in the microtubule lattice activate GEF-H1-dependent RhoA signalling.Nature cell biology · 2026Article
- Charcot-Marie-Tooth disease and related neuropathies.Nature reviews. Disease primers · 2026Review
- Mechanical regulation of metabolism, epigenetics, and their interplay.npj biomedical innovations · 2026Review
- Swelling-induced calcium signaling in wild-type andFrontiers in cellular neuroscience · 2026Article
- Direct crosstalk between GPCRs and ion channels via G proteins.Experimental & molecular medicine · 2025Review
- Targeting TRPV4 to restore glymphatic system function and alleviate cerebral edema in ischemic stroke.Brain pathology (Zurich, Switzerland) · 2025Article
- Enhanced neuromorphogenesis of neural stem cells via the optimization of physical stimulus-responsive signaling pathways.Stem cell research & therapy · 2025Article
- TRPV4 controls circadian and pathological ocular hypertension.The Journal of physiology · 2025Article
- TRPV4 Channel in Neurological Disease: from Molecular Mechanisms to Therapeutic Potential.Molecular neurobiology · 2025Review
- Combined clinical, structural and cellular studies discriminate pathogenic and benign TRPV4 variants.Brain : a journal of neurology · 2025Article
- Forty sites of TRP channel regulation.Current opinion in chemical biology · 2025Review
- TRPV4 neuromuscular disease registry highlights bulbar, skeletal and proximal limb manifestations.Brain : a journal of neurology · 2025Article
- Recent advances on the structure and the function relationships of the TRPV4 ion channel.Channels (Austin, Tex.) · 2024Review
- Clinical and Genetic Profiles of 5q- and Non-5q-Spinal Muscular Atrophy Diseases in Pediatric Patients.Genes · 2024Review
- TRPV4 subserves physiological and pathological elevations in intraocular pressure.Research square · 2024Article
- Structural Pharmacology of TRPV4 Antagonists.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Gain-of-function mutations of TRPV4 acting in endothelial cells drive blood-CNS barrier breakdown and motor neuron degeneration in mice.Science translational medicine · 2024Article
- Structural insights into the TRPV4-RhoA complex offer clues to solve the puzzle of TRPV4 channelopathies.Cell calcium · 2023Article
- Crosstalk between regulatory elements in disordered TRPV4 N-terminus modulates lipid-dependent channel activity.Nature communications · 2023Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
Abstract
TRPV4 is a cell surface-expressed calcium-permeable cation channel that mediates cell-specific effects on cellular morphology and function. Dominant missense mutations of TRPV4 cause distinct, tissue-specific diseases, but the pathogenic mechanisms are unknown. Mutations causing peripheral neuropathy localize to the intracellular N-terminal domain whereas skeletal dysplasia mutations are in multiple domains. Using an unbiased screen, we identified the cytoskeletal remodeling GTPase RhoA as a TRPV4 interactor. TRPV4-RhoA binding occurs via the TRPV4 N-terminal domain, resulting in suppression of TRPV4 channel activity, inhibition of RhoA activation, and extension of neurites in vitro. Neuropathy but not skeletal dysplasia mutations disrupt TRPV4-RhoA binding and cytoskeletal outgrowth. However, inhibition of RhoA restores neurite length in vitro and in a fly model of TRPV4 neuropathy. Together these results identify RhoA as a critical mediator of TRPV4-induced cell structure changes and suggest that disruption of TRPV4-RhoA binding may contribute to tissue-specific toxicity of TRPV4 neuropathy mutations.
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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.