Zusammenfassung
Oxidativer Stress am retinalen Pigmentepithel (RPE) ist ursächlich an der Entstehung der altersbedingten Makuladegeneration (AMD) beteiligt. Ein Oxidationsschutz des RPE durch Supplementation von Antioxidantien ist sowohl auf klinischer als auch auf experimenteller Ebene komplex. Ein mögliches therapeutisches Target ist die durch oxidativen Stress angestoßene zelluläre Signaltransduktion, an deren Ende z. B. eine veränderte Expression von vasoaktiven Signalmolekülen oder die Induktion von Apoptose steht. Die Übersichtsarbeit fasst den Stand der Literatur zu zellulären Effekten freier Radikale zusammen und leitet daraus mögliche Ansätze zur therapeutischen Protektion des RPE ab.
Abstract
Oxidative stress at the retinal pigment epithelium (RPE) is involved in the pathophysiology of age-related macula degeneration (ARMD). Observations on a clinical or laboratory level have revealed that supplementation of antioxidative scavengers failed in many cases. A potential therapeutic target is the cellular signal transduction cascade initiated by oxidative stress which results, e. g., in altered expression of pro- and antiagiogenic factors as well as induction of apoptosis. This review summarises the current literature on cellular effects of free radicals and deduces potential therapeutic approaches to protect the RPE from oxidative damage.
Schlüsselwörter
Retina - Pharmakologie - Pathologie
Key words
Retina - Pharmacology - Pathology
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PD Dr. Oliver Zeitz
Klinik und Poliklinik für Augenheilkunde, Universitätsklinikum Hamburg-Eppendorf
Martinistr. 52
20246 Hamburg
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