[Molecular mechanisms of retinal ischemia].
The review discusses the molecular mechanisms of retinal damage, which are associated with retinal ischemia. Ischemia is one of the key factors determining the pathophysiology of many retinal diseases, such as diabetic retinopathy, glaucoma, anterior ischemic optic neuropathy, age-related macular degeneration, retinopathy of prematurity. Hypoxia and ischemia impair retinal neuronal energy metabolism, by launching a cascade of trigger reactions resulting in cell death. Oxidative stress, excitotoxicity, cell acidosis, inflammation, and others mechanisms acting in tandem are of considerable importance in ischemia. Neuronal apoptosis and neovascularization are the most important sequels of ischemia. Among all retinal neurons, ganglion cells are most susceptible to ischemia, which determines their early structural and functional changes in many ischemia-associated retinal diseases. The molecular mechanisms underlying the pathophysiology of ischemia-associated retinal diseases should be understood to substantiate and develop new therapy modalities.
Neroev
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VV
Zueva
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MV
Kalamkarov
G R
GR
D017209:Apoptosis; D018698:Glutamic Acid / Q000378:metabolism; D006801:Humans; D007511:Ischemia / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D009389:Neovascularization, Pathologic / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D009569:Nitric Oxide / Q000378:metabolism; D018384:Oxidative Stress; D012160:Retina / Q000378:metabolism / Q000473:pathology; D012164:Retinal Diseases / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D055351:Retinal Neurons / Q000378:metabolism / Q000473:pathology; D012171:Retinal Vessels / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology
D009569:Nitric Oxide; D018698:Glutamic Acid