ReviewExperimental eye research2009
The role of proteolytic cellular systems in trabecular meshwork homeostasis.
Review in Experimental eye research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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
21 citing papers in PubMed, 34 citations in OpenAlex.
- Macular Thickness and Its Associated Factors in a Healthy Cynomolgus Colony: The Non-Human Primates Eye Study.Ophthalmology science · 2026Article
- The Interplay Between the Ubiquitin-Proteasome System and Oxidative Stress: A Future Perspective in Eye Diseases.Antioxidants (Basel, Switzerland) · 2025Review
- Aging and intraocular pressure homeostasis in mice.Aging cell · 2024Article
- PBX1 attenuates HCell stress & chaperones · 2022Article
- Cell senescence alters responses of porcine trabecular meshwork cells to shear stress.Frontiers in cell and developmental biology · 2022Article
- Dexamethasone Downregulates Autophagy through Accelerated Turn-Over of the Ulk-1 Complex in a Trabecular Meshwork Cells Strain: Insights on Steroid-Induced Glaucoma Pathogenesis.International journal of molecular sciences · 2021Article
- Secreted protein acidic and rich in cysteine (SPARC) knockout mice have greater outflow facility.PloS one · 2020Article
- Working your SOCS off: The role of ASB10 and protein degradation pathways in glaucoma.Experimental eye research · 2017Review
- Steroid-induced ocular hypertension/glaucoma: Focus on pharmacogenomics and implications for precision medicine.Progress in retinal and eye research · 2017Review
- Transplantation of iPSC-derived TM cells rescues glaucoma phenotypes in vivo.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- The autophagic lysosomal system in outflow pathway physiology and pathophysiology.Experimental eye research · 2016Review
- Glaucomatous MYOC mutations activate the IL-1/NF-κB inflammatory stress response and the glaucoma marker SELE in trabecular meshwork cells.Molecular vision · 2015Article
- Canonical wnt signaling regulates extracellular matrix expression in the trabecular meshwork.Investigative ophthalmology & visual science · 2014Article
- AMP-activated protein kinase regulates intraocular pressure, extracellular matrix, and cytoskeleton in trabecular meshwork.Investigative ophthalmology & visual science · 2014Article
- Overexpression of SPARC in human trabecular meshwork increases intraocular pressure and alters extracellular matrix.Investigative ophthalmology & visual science · 2013Article
- Oxidative stress response signaling pathways in trabecular meshwork cells and their effects on cell viability.Molecular vision · 2013Article
- Prenylation of Rho G-proteins: a novel mechanism regulating gene expression and protein stability in human trabecular meshwork cells.Molecular neurobiology · 2012Article
- Current understanding of conventional outflow dysfunction in glaucoma.Current opinion in ophthalmology · 2012Review
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Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The molecular mechanisms contributing to the progressive malfunction of the trabecular meshwork (TM)/Schlemm's canal (SC) conventional outflow pathway during aging and in Primary Open Angle Glaucoma (POAG) are still poorly understood. Progressive accumulation of damaged and cross-linked proteins is a hallmark of aging tissues and has been proposed to play a major role in the tissue abnormalities associated with organismal aging and many age-related diseases. Such progressive accumulation of damaged proteins with age is believed to result from both, increased oxidative stress that results in faster rates of protein damage, as well as from a functional decline in the cellular proteolytic machinery that eliminates misfolded and damaged proteins. Here, we review the reported data that supports the occurrence of oxidative damage and the alterations in the intracellular proteolytic systems in the TM in aging and POAG. Finally, we discuss how the functional decline of the cellular proteolytic machinery in the TM might lead to the observed physiologic alterations of the outflow pathway in glaucoma.
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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.