ArticleJournal of cellular physiology2022
Novel insight into the role of clusterin on intraocular pressure regulation by modifying actin polymerization and extracellular matrix remodeling in the trabecular meshwork.
Article in Journal of cellular physiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
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Who cites it
15 citing papers in PubMed, 22 citations in OpenAlex.
- Isobaric quantitative proteomics reveals altered extracellular matrix, cytoskeletal, and degradation pathways in glaucomatous trabecular meshwork cells.Scientific reports · 2026Article
- Clusterin reverses epitheliopathy, reduces inflammation, and restores goblet cells and corneal nerves in a mouse model of autoimmune dry eye.Scientific reports · 2026Article
- Loss of Cathepsin K Impairs Collagen Biogenesis and Enhances Actin Polymerization in Trabecular Meshwork.Investigative ophthalmology & visual science · 2026Article
- Co-delivery of ripasudil and dexamethasone in trabecular meshwork cells for potential prevention of GC-induced ocular hypertension.Experimental cell research · 2025Article
- Lipids and lipid regulators in intraocular pressure homeostasis.Current opinion in pharmacology · 2025Review
- High Glucose-induced transcriptomic changes in human trabecular meshwork cells.Molecular biology reports · 2025Article
- Regulatory role of cholesterol in modulating actin dynamics and cell adhesive interactions in the trabecular meshwork.bioRxiv : the preprint server for biology · 2024Article
- Method to Assess the Intracellular Fate and Bioavailability of Clusterin Using Live Cell Confocal Microscopy Imaging.Methods in molecular biology (Clifton, N.J.) · 2024Article
- Identification of the novel role of sterol regulatory element binding proteins (SREBPs) in mechanotransduction and intraocular pressure regulation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2023Article
- Glaucoma: Novel antifibrotic therapeutics for the trabecular meshwork.European journal of pharmacology · 2023Review
- Characterization of extracellular matrix deposited by segmental trabecular meshwork cells.Experimental eye research · 2023Article
- The normalizing effects of the CYP46A1 activator efavirenz on retinal sterol levels and risk factors for glaucoma in ApojCellular and molecular life sciences : CMLS · 2023Article
- Characterization of extracellular matrix deposited by segmental trabecular meshwork cells.bioRxiv : the preprint server for biology · 2023Article
- Extracellular-Matrix Mechanics Regulate the Ocular Physiological and Pathological Activities.Journal of ophthalmology · 2023Review
- Novel insight into the role of clusterin on intraocular pressure regulation by modifying actin polymerization and extracellular matrix remodeling in the trabecular meshwork.Journal of cellular physiology · 2022Article
Corrections and comments
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Authors and funding
5 authors at 4 institutions in 1 country.
Funding
Abstract
This study provides comprehensive mechanistic evidence for the role of clusterin, a stress-response secretory chaperone protein, in the modulation of intraocular pressure (IOP) by regulating the trabecular meshwork (TM) actin cytoskeleton and the extracellular matrix (ECM). The pathological stressors on TM known to elevate IOP significantly lowered clusterin protein levels indicating stress-related clusterin function loss. Small interfering RNA-mediated clusterin loss in human TM cells in vitro induced actin polymerization and stabilization via protein kinase D1, serine/threonine-protein kinase N2 (PRK2), and LIM kinase 1 (LIMK1), and the recruitment and activation of adhesome proteins including paxillin, vinculin, and integrin αV and β5. A complete loss of clusterin as seen in clusterin knockout mice (Clu
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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 Socratic graph.