ArticleiScience2021
The role of Piezo1 in conventional aqueous humor outflow dynamics.
Article in iScience, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
What it found
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Who cites it
30 citing papers in PubMed, 44 citations in OpenAlex.
- TRPV4 regulates intraocular pressure through trabecular meshwork contractility and fibrosis.Channels (Austin, Tex.) · 2026Review
- Piezo1 Activation by Shear Stress Induces Corneal Epithelial Homeostasis Disruption.Investigative ophthalmology & visual science · 2026Article
- Transformative biomechanics and mechanobiology breakthroughs shaping the future of health and medicine.Innovation (Cambridge (Mass.)) · 2026Review
- PIEZO channels in the eye: unveiling a mechanical code in ocular physiology and disease.Science China. Life sciences · 2025Article
- Pericytes in the optic nerve head.Progress in retinal and eye research · 2025Review
- TRPV4 controls circadian and pathological ocular hypertension.The Journal of physiology · 2025Article
- TRPV4 activation by TGFβ2 enhances cellular contractility and drives ocular hypertension.eLife · 2025Article
- Mechanobiology in the eye.npj biological physics and mechanics · 2025Review
- Piezo in the eye: expression, distribution and roles in ocular diseases.Frontiers in physiology · 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
- Mechanosensitive ion channels in glaucoma pathophysiology.Vision research · 2024Review
- Influence of Intraocular Pressure on the Expression and Activity of Sodium-Potassium Pumps in the Corneal Endothelium.International journal of molecular sciences · 2024Article
- Resting human trabecular meshwork cells experience tonic cation influx.Research square · 2024Article
- TRPV4 subserves physiological and pathological elevations in intraocular pressure.Research square · 2024Article
- Role of mechanically-sensitive cation channels Piezo1 and TRPV4 in trabecular meshwork cell mechanotransduction.Human cell · 2024Review
- Assessment of corneal nerve regeneration after axotomy in a compartmentalized microfluidic chip model with automated 3D high resolution live-imaging.Frontiers in cellular neuroscience · 2024Article
- Differential expression of PIEZO1 and PIEZO2 mechanosensitive channels in ocular tissues implicates diverse functional roles.Experimental eye research · 2023Article
- Mechanosensitive ion channel gene survey suggests potential roles in primary open angle glaucoma.Scientific reports · 2023Article
- Slowed Intestinal Transit Induced by Less Mucus in Intestinal Goblet Cell Piezo1-Deficient Mice through Impaired Epithelial Homeostasis.International journal of molecular sciences · 2023Article
Corrections and comments
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Authors and funding
18 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Controlling intraocular pressure (IOP) remains the mainstay of glaucoma therapy. The trabecular meshwork (TM), the key tissue responsible for aqueous humor (AH) outflow and IOP maintenance, is very sensitive to mechanical forces. However, it is not understood whether Piezo channels, very sensitive mechanosensors, functionally influence AH outflow. Here, we characterize the role of Piezo1 in conventional AH outflow. Immunostaining and western blot analysis showed that Piezo1 is widely expressed by TM. Patch-clamp recordings in TM cells confirmed the activation of Piezo1-derived mechanosensitive currents. Importantly, the antagonist GsMTx4 for mechanosensitive channels significantly decreased steady-state facility, yet activation of Piezo1 by the specific agonist Yoda1 did not lead to a facility change. Furthermore, GsMTx4, but not Yoda1, caused a significant increase in ocular compliance, a measure of the eye's transient response to IOP perturbation. Our findings demonstrate a potential role for Piezo1 in conventional outflow, likely under pathological and rapid transient conditions.
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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.