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DOI: 10.1055/a-2063-8957
Die Blut-Augen-Schranken und ihre Störungen: Anatomie, Physiologie, Pathologie
Article in several languages: deutsch | EnglishZusammenfassung
Die Blut-Augen-Schranken, bestehend aus Blut-Kammerwasser-Schranke (BKS) und Blut-Retina-Schranke (BRS), bilden eine selektiv permeable physiologische Barriere zwischen der stark vaskularisierten Uvea und dem Vorderkammer- und Glaskörperraum sowie der sensorischen Netzhaut aus. Diese Barrieren schützen vor dem Eindringen von Toxinen und Krankheitserregern aus dem Blutkreislauf, kontrollieren den Protein- und Flüssigkeitshaushalt und tragen aktiv zum Erhalt des okulären Immunprivilegs bei. Morphologisches Korrelat der Blut-Augen-Schranken sind Tight Junctions zwischen benachbarten Endothel- und Epithelzellen, die den Interzellularraum abdichten und eine unkontrollierte parazelluläre Diffusion von Molekülen verhindern. Die BKS besteht aus den Tight Junctions der Endothelzellen der Irisgefäße, der Endothelzellen der Innenwand des Schlemm-Kanals und der Epithelzellen des unpigmentierten Ziliarepithels; die BRS setzt sich aus den Tight Junctions der Endothelzellen der retinalen Gefäße (innere BRS) und des retinalen Pigmentepithels (äußere BRS) zusammen. Während endotheliale Schranken eine absolute immunologische Barriere darstellen, fungieren epitheliale Schranken als immunregulatorische „Gatekeeper“, die Leukozyten kontrolliert passieren lassen. Funktionelle Störungen der Blut-Augen-Schranken, klinisch messbar mittels Laser-Flare-Photometrie oder Fluorophotometrie, können im Rahmen traumatischer, entzündlicher und infektiöser Prozesse auftreten, sind aber auch an der Pathophysiologie chronischer Erkrankungen des vorderen Augenabschnitts, wie Glaukom, und der Netzhaut, wie diabetischer Retinopathie und altersbedingter Makuladegeneration, zentral beteiligt.
Schlüsselwörter
Blut-Augen-Schranken - Blut-Kammerwasser-Schranke - Blut-Retina-Schranke - Tight Junctions - diabetische Retinopathie - altersbedingte MakuladegenerationPublication History
Received: 05 January 2023
Accepted: 21 March 2023
Article published online:
19 May 2023
© 2023. Thieme. All rights reserved.
Georg Thieme Verlag KG
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