Mitochondrial complex I defect induces ROS release and degeneration in trabecular meshwork cells of POAG patients: protection by antioxidants. - Wikidata - wikimedia - TriplyDB

Mitochondrial complex I defect induces ROS release and degeneration in trabecular meshwork cells of POAG patients: protection by antioxidants.

Mitochondrial complex I defect induces ROS release and degeneration in trabecular meshwork cells of POAG patients: protection by antioxidants.

http://www.wikidata.org/entity/Q46667385

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Neuroprotection in Glaucoma Mitochondrial pathogenic mechanism and degradation in optineurin E50K mutation-mediated retinal ganglion cell degeneration Erythropoietin protects cardiomyocytes from cell death during hypoxia/reperfusion injury through activation of survival signaling pathways Evaluation of an injectable thermosensitive hydrogel as drug delivery implant for ocular glaucoma surgery Cardiolipin promotes electron transport between ubiquinone and complex I to rescue PINK1 deficiency The Eye Drop Preservative Benzalkonium Chloride Potently Induces Mitochondrial Dysfunction and Preferentially Affects LHON Mutant Cells Dexamethasone disrupts intercellular junction formation and cytoskeleton organization in human trabecular meshwork cells.Variability of serum oxidative stress biomarkers relative to biochemical data and clinical parameters of glaucoma patients 4-methylene-2-octyl-5-oxotetrahydrofuran-3-carboxylic acid (C75), an inhibitor of fatty-acid synthase, suppresses the mitochondrial fatty acid synthesis pathway and impairs mitochondrial function Mitochondrial damage in the trabecular meshwork occurs only in primary open-angle glaucoma and in pseudoexfoliative glaucoma Down-regulation of GRP78 in human glaucomatous trabecular meshwork cells.Decreased carbohydrate metabolism enzyme activities in the glaucomatous trabecular meshwork Preventive effects of omega-3 and omega-6 Fatty acids on peroxide mediated oxidative stress responses in primary human trabecular meshwork cells.A laser-induced mouse model with long-term intraocular pressure elevation.A narrative review on the similarities and dissimilarities between myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) and sickness behavior.The ocular hypotensive effect of saffron extract in primary open angle glaucoma: a pilot study Helicobacter pylori infection and eye diseases: a systematic review.The mitochondrial complex I activity is reduced in cells with impaired cystic fibrosis transmembrane conductance regulator (CFTR) function.ES micro-environment enhances stemness and inhibits apoptosis in human limbal stem cells via the maintenance of telomerase activity Intralysosomal iron induces lysosomal membrane permeabilization and cathepsin D-mediated cell death in trabecular meshwork cells exposed to oxidative stress.Mitochondrial genome analysis of primary open angle glaucoma patients Focus on molecular events in the anterior chamber leading to glaucoma.Mitochondrial sequence variation in African-American primary open-angle glaucoma patients Premature aging with impaired oxidative stress defense in mice lacking TR4.Increased mitochondrial fission and volume density by blocking glutamate excitotoxicity protect glaucomatous optic nerve head astrocytes.Quantitative proteomics: TGFβ₂ signaling in trabecular meshwork cells.Measurement of Systemic Mitochondrial Function in Advanced Primary Open-Angle Glaucoma and Leber Hereditary Optic Neuropathy.Multipotent stem cells from trabecular meshwork become phagocytic TM cells.Adeno-associated virus mediated SOD gene therapy protects the retinal ganglion cells from chronic intraocular pressure elevation induced injury via attenuating oxidative stress and improving mitochondrial dysfunction in a rat model.Mitochondria impairment correlates with increased sensitivity of aging RPE cells to oxidative stress.Proteomic similarities in steroid responsiveness in normal and glaucomatous trabecular meshwork cells Stem cells from trabecular meshwork home to TM tissue in vivo.Current primary open-angle glaucoma treatments and future directions.PRDX6 attenuates oxidative stress- and TGFbeta-induced abnormalities of human trabecular meshwork cells.The autophagic lysosomal system in outflow pathway physiology and pathophysiology.Lysosomal basification and decreased autophagic flux in oxidatively stressed trabecular meshwork cells: implications for glaucoma pathogenesis.Heat shock proteins in the retina: Focus on HSP70 and alpha crystallins in ganglion cell survival.Association of primary open-angle glaucoma with mitochondrial variants and haplogroups common in African Americans.Pro370Leu mutant myocilin impairs mitochondrial functions in human trabecular meshwork cells.Inhibition of oxidative stress by coenzyme Q10 increases mitochondrial mass and improves bioenergetic function in optic nerve head astrocytes.

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P2860

Mitochondrial complex I defect induces ROS release and degeneration in trabecular meshwork cells of POAG patients: protection by antioxidants.

http://www.wikidata.org/entity/Q46667385

description

2008 nî lūn-bûn

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2008年の論文

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2008年学术文章

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2008年学术文章

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2008年学术文章

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2008年学术文章

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2008年学术文章

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2008年学术文章

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2008年學術文章

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2008年學術文章

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Mitochondrial complex I defect ...... s: protection by antioxidants.

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Mitochondrial complex I defect ...... s: protection by antioxidants.

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type

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Mitochondrial complex I defect ...... s: protection by antioxidants.

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Mitochondrial complex I defect ...... s: protection by antioxidants.

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Mitochondrial complex I defect ...... s: protection by antioxidants.

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Mitochondrial complex I defect ...... s: protection by antioxidants.

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Jian Ge

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Joyce Tombran-Tink

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Kar Wah Leung

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Ru-Zhang Jiang

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Shan Duan

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Xiu-Feng Zhong

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Yuan He

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Yue-Hong Zhang

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Zhan Peng

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1447-1458

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10.1167/IOVS.07-1361

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4

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2008-04-01T00:00:00Z

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18385062

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