ArticleJournal of cellular and molecular medicine2020
AQP1 suppression by ATF4 triggers trabecular meshwork tissue remodelling in ET-1-induced POAG.
Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
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Who cites it
16 citing papers in PubMed, 19 citations in OpenAlex.
- Targeting Circadian Rhythm Disruption in Glaucoma: PTGDS Mediates Trabecular Meshwork Fibrosis and Is Therapeutically Targeted by Aprepitant.Translational vision science & technology · 2026Article
- Effective Component Compatibility of Bufei Yishen Formula III Alleviates Pulmonary Vascular Inflammation in COPD: Via VEGFJournal of inflammation research · 2026Article
- Aquaporin-1 upregulation is associated with scleral remodeling during myopia development in mice.American journal of translational research · 2026Article
- The characteristics of fundus microvascular alterations in the course of glaucoma: a narrative review.Annals of translational medicine · 2022Review
- Cellular stress signaling and the unfolded protein response in retinal degeneration: mechanisms and therapeutic implications.Molecular neurodegeneration · 2022Review
- Signaling Mechanisms and Pharmacological Modulators Governing Diverse Aquaporin Functions in Human Health and Disease.International journal of molecular sciences · 2022Review
- Degeneration of retina-brain components and connections in glaucoma: Disease causation and treatment options for eyesight preservation.Current research in neurobiology · 2022Review
- Magnesium and Its Role in Primary Open Angle Glaucoma; A Novel Therapeutic?Frontiers in ophthalmology · 2022Review
- Fundamental Biomaterial Considerations in the Development of a 3D Model Representative of Primary Open Angle Glaucoma.Bioengineering (Basel, Switzerland) · 2021Review
- TACR2 is associated with the immune microenvironment and inhibits migration and proliferation via the Wnt/β-catenin signaling pathway in prostate cancer.Cancer cell international · 2021Article
- Crosstalk between MicroRNA and Oxidative Stress in Primary Open-Angle Glaucoma.International journal of molecular sciences · 2021Review
- Network Integration Analysis and Immune Infiltration Analysis Reveal Potential Biomarkers for Primary Open-Angle Glaucoma.Frontiers in cell and developmental biology · 2021Article
- Therapeutic Drugs and Devices for Tackling Ocular Hypertension and Glaucoma, and Need for Neuroprotection and Cytoprotective Therapies.Frontiers in pharmacology · 2021Review
- Analysis of the Responsiveness of Latanoprost, Travoprost, Bimatoprost, and Tafluprost in the Treatment of OAG/OHT Patients.Journal of ophthalmology · 2021Review
- Neuroinflammation in Primary Open-Angle Glaucoma.Journal of clinical medicine · 2020Review
- AQP1 suppression by ATF4 triggers trabecular meshwork tissue remodelling in ET-1-induced POAG.Journal of cellular and molecular medicine · 2020Article
Corrections and comments
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Authors and funding
14 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Primary open-angle glaucoma (POAG) is the second leading cause of irreversible blindness worldwide. Increased endothelin-1 (ET-1) has been observed in aqueous humour (AH) of POAG patients, resulting in an increase in the out-flow resistance of the AH. However, the underlining mechanisms remain elusive. Using established in vivo and in vitro POAG models, we demonstrated that water channel Aquaporin 1 (AQP1) is down-regulated in trabecular meshwork (TM) cells upon ET-1 exposure, which causes a series of glaucomatous changes, including actin fibre reorganization, collagen production, extracellular matrix deposition and contractility alteration of TM cells. Ectopic expression of AQP1 can reverse ET-1-induced TM tissue remodelling, which requires the presence of β-catenin. More importantly, we found that ET-1-induced AQP1 suppression is mediated by ATF4, a transcription factor of the unfolded protein response, which binds to the promoter of AQP1 and negatively regulates AQP1 transcription. Thus, we discovered a novel function of ATF4 in controlling the process of TM remodelling in ET-1-induced POAG through transcription suppression of AQP1. Our findings also detail a novel pathological mechanism and a potential therapeutic target for POAG.
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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.