Mechanisms of Retinal Ganglion Cell Injury in Aging and Glaucoma
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作者:
Chrysostomou, Vicki
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Univ Melbourne, Ctr Eye Res Australia, Glaucoma Res Unit, Royal Victorian Eye & Ear Hosp,Dept Ophthalmol, Melbourne, Vic 3002, AustraliaUniv Melbourne, Ctr Eye Res Australia, Glaucoma Res Unit, Royal Victorian Eye & Ear Hosp,Dept Ophthalmol, Melbourne, Vic 3002, Australia
Chrysostomou, Vicki
[1
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Trounce, Ian A.
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Univ Melbourne, Ctr Eye Res Australia, Glaucoma Res Unit, Royal Victorian Eye & Ear Hosp,Dept Ophthalmol, Melbourne, Vic 3002, AustraliaUniv Melbourne, Ctr Eye Res Australia, Glaucoma Res Unit, Royal Victorian Eye & Ear Hosp,Dept Ophthalmol, Melbourne, Vic 3002, Australia
Trounce, Ian A.
[1
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Crowston, Jonathan G.
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Univ Melbourne, Ctr Eye Res Australia, Glaucoma Res Unit, Royal Victorian Eye & Ear Hosp,Dept Ophthalmol, Melbourne, Vic 3002, AustraliaUniv Melbourne, Ctr Eye Res Australia, Glaucoma Res Unit, Royal Victorian Eye & Ear Hosp,Dept Ophthalmol, Melbourne, Vic 3002, Australia
Crowston, Jonathan G.
[1
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[1] Univ Melbourne, Ctr Eye Res Australia, Glaucoma Res Unit, Royal Victorian Eye & Ear Hosp,Dept Ophthalmol, Melbourne, Vic 3002, Australia
Aging is the greatest risk factor for glaucoma, implying that intrinsic age-related changes to retinal ganglion cells, their supporting tissue or both make retinal ganglion cells susceptible to injury. Changes to the ocular vasculature, connective tissue of the optic nerve head and mitochondria, which have been documented with advancing age and shown to be exacerbated in glaucoma, may predispose to glaucomatous injury. When considering such age-related changes, it is difficult to separate pathological change from physiological change, and cause from consequence. The insults that predispose aged retinal ganglion cells to injury are likely to be varied and multiple; therefore, it may be more relevant to identify and treat common mechanisms that predispose to retinal ganglion cell failure and/or death. We suggest that mitochondrial dysfunction, as either a cause or consequence of injury, renders retinal ganglion cells sensitive to degeneration. Therapeutic approaches that target mitochondria and promote energy production may provide a general means of protecting aged retinal ganglion cells from degeneration, regardless of the etiology. Copyright (C) 2010 S. Karger AG, Basel
机构:
Chaim Sheba Med Ctr, Goldschleger Eye Inst, Glaucoma Serv, IL-52621 Tel Hashomer, Israel
Tel Aviv Univ, Sackler Fac Med, IL-52621 Tel Hashomer, IsraelChaim Sheba Med Ctr, Goldschleger Eye Inst, Glaucoma Serv, IL-52621 Tel Hashomer, Israel
Levkovitch-Verbin, Hani
NEW TRENDS IN BASIC AND CLINICAL RESEARCH OF GLAUCOMA: A NEURODEGENERATIVE DISEASE OF THE VISUAL SYSTEM, PT A,
2015,
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