ArticleScientific reports2016
TRPV4 regulates calcium homeostasis, cytoskeletal remodeling, conventional outflow and intraocular pressure in the mammalian eye.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 97 papers.
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Who cites it
97 citing papers in PubMed, 137 citations in OpenAlex.
- TRPV4 regulates intraocular pressure through trabecular meshwork contractility and fibrosis.Channels (Austin, Tex.) · 2026Review
- Investigating the coupled effects of stiffness and stretch on the trabecular meshwork cells using a hydrogel-integrated microfluidic system.Biomaterials science · 2026Article
- 25+ Years of TRPV4: From Discovery to Translational Horizons.Research square · 2026Article
- Shear Stress as a Driver of Retinal Müller Glia Survival and Fibrotic Reprogramming.Cell biochemistry and function · 2026Article
- Bioengineered 3D Human Trabecular Meshwork Models for Outflow Physiology and Glaucoma Research.Bioengineering (Basel, Switzerland) · 2026Review
- The TRPV4-YAP axis mediates cytoskeletal and extracellular matrix remodeling in trabecular meshwork cells as a novel glaucoma mechanism.Scientific reports · 2025Article
- Mechano- and Glucocorticoid-Sensitive TREK-1 Channels Regulate Conventional Outflow and Intraocular Pressure.Investigative ophthalmology & visual science · 2025Article
- Intraocular pressure variation (ocular hypertension) in diabetes mellitus.World journal of clinical cases · 2025Review
- Transient receptor potential vanilloid 4 modulates substrate stiffness mechanosensing and transcellular pore formation in human Schlemm's canal cells.Acta biomaterialia · 2025Article
- Substrate stiffness and pressure alter retinal Müller glia response and extracellular matrix production.Biomaterials and biosystems · 2025Article
- TRPV4 controls circadian and pathological ocular hypertension.The Journal of physiology · 2025Article
- Methods for Mitochondrial DNA Damage and Depletion in Immortalized Trabecular Meshwork Cells.International journal of molecular sciences · 2025Article
- TRPV4 activation by TGFβ2 enhances cellular contractility and drives ocular hypertension.eLife · 2025Article
- Biomechanical properties of the trabecular meshwork in intraocular pressure regulation: a review.International ophthalmology · 2025Review
- TRPV4 modulates substrate stiffness mechanosensing and transcellular pore formation in human Schlemm's canal cells.bioRxiv : the preprint server for biology · 2025Article
- Neuropsin, TRPV4 and intracellular calcium mediate intrinsic photosensitivity in corneal epithelial cells.The ocular surface · 2025Article
- TRPV4 modulates inflammatory responses and apoptosis in enteric glial cells triggered by Clostridioides difficile toxins A and B.Journal of inflammation (London, England) · 2025Article
- Mechanobiology in the eye.npj biological physics and mechanics · 2025Review
- Ion channel Piezo1 induces ferroptosis of trabecular meshwork cells: a novel observation in the pathogenesis in primary open angle glaucoma.American journal of physiology. Cell physiology · 2024Article
- Resting trabecular meshwork cells experience constitutive cation influx.Vision research · 2024Article
37 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
14 authors at 2 institutions in 1 country.
Funding
Abstract
An intractable challenge in glaucoma treatment has been to identify druggable targets within the conventional aqueous humor outflow pathway, which is thought to be regulated/dysregulated by elusive mechanosensitive protein(s). Here, biochemical and functional analyses localized the putative mechanosensitive cation channel TRPV4 to the plasma membrane of primary and immortalized human TM (hTM) cells, and to human and mouse TM tissue. Selective TRPV4 agonists and substrate stretch evoked TRPV4-dependent cation/Ca(2+) influx, thickening of F-actin stress fibers and reinforcement of focal adhesion contacts. TRPV4 inhibition enhanced the outflow facility and lowered perfusate pressure in biomimetic TM scaffolds populated with primary hTM cells. Systemic delivery, intraocular injection or topical application of putative TRPV4 antagonist prodrug analogs lowered IOP in glaucomatous mouse eyes and protected retinal neurons from IOP-induced death. Together, these findings indicate that TRPV4 channels function as a critical component of mechanosensitive, Ca(2+)-signaling machinery within the TM, and that TRPV4-dependent cytoskeletal remodeling regulates TM stiffness and outflow. Thus, TRPV4 is a potential IOP sensor within the conventional outflow pathway and a novel target for treating ocular hypertension.
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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.