ArticleCells2021
Cathepsin K Regulates Intraocular Pressure by Modulating Extracellular Matrix Remodeling and Actin-Bundling in the Trabecular Meshwork Outflow Pathway.
Article in Cells, 2021. 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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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
15 citing papers in PubMed, 21 citations in OpenAlex.
- Chromatin dynamics identifies 78 genes at loci associated with elevated intraocular pressure and primary open-angle glaucoma.bioRxiv : the preprint server for biology · 2026Article
- Loss of Cathepsin K Impairs Collagen Biogenesis and Enhances Actin Polymerization in Trabecular Meshwork.Investigative ophthalmology & visual science · 2026Article
- Sustained release of cathepsin D/cathepsin K from injectable hydrogel microspheres in anti-photoaging.Materials today. Bio · 2025Article
- Prediction of Bioactive Metabolites from AmericanJournal of natural products · 2025Article
- 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
- scAAV2-Mediated Expression of Thioredoxin 2 and C3 Transferase Prevents Retinal Ganglion Cell Death and Lowers Intraocular Pressure in a Mouse Model of Glaucoma.International journal of molecular sciences · 2023Article
- 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
- Sigma-1 Receptor Agonist Fluvoxamine Ameliorates Fibrotic Response of Trabecular Meshwork Cells.International journal of molecular sciences · 2023Article
- Biodegradation of Dental Resin-Based Composite-A Potential Factor Affecting the Bonding Effect: A Narrative Review.Biomedicines · 2022Review
- The physiological and pathophysiological roles of the autophagy lysosomal system in the conventional aqueous humor outflow pathway: More than cellular clean up.Progress in retinal and eye research · 2022Review
- 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
- Genome-wide association study finds multiple loci associated with intraocular pressure in HS rats.Frontiers in genetics · 2022Article
- The role of Vitamin D3 in ocular fibrosis and its therapeutic potential for the glaucomatous trabecular meshwork.Frontiers in ophthalmology · 2022Review
- Age-Related Alterations of Hyaluronan and Collagen in Extracellular Matrix of the Muscle Spindles.Journal of clinical medicine · 2021Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
The homeostasis of extracellular matrix (ECM) and actin dynamics in the trabecular meshwork (TM) outflow pathway plays a critical role in intraocular pressure (IOP) regulation. We studied the role of cathepsin K (CTSK), a lysosomal cysteine protease and a potent collagenase, on ECM modulation and actin cytoskeleton rearrangements in the TM outflow pathway and the regulation of IOP. Initially, we found that CTSK was negatively regulated by pathological stressors known to elevate IOP. Further, inactivating CTSK using balicatib, a pharmacological cell-permeable inhibitor of CTSK, resulted in IOP elevation due to increased levels and excessive deposition of ECM-like collagen-1A in the TM outflow pathway. The loss of CTSK activity resulted in actin-bundling via fascin and vinculin reorganization and by inhibiting actin depolymerization via phospho-cofilin. Contrarily, constitutive expression of CTSK decreased ECM and increased actin depolymerization by decreasing phospho-cofilin, negatively regulated the availability of active TGFβ2, and reduced the levels of alpha-smooth muscle actin (αSMA), indicating an antifibrotic action of CTSK. In conclusion, these observations, for the first time, demonstrate the significance of CTSK in IOP regulation by maintaining the ECM homeostasis and actin cytoskeleton-mediated contractile properties of the TM outflow pathway.
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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.