Kallikrein-kinin activation by altered vitreous pH: New perspectives for treatment and pathogenesis of diabetic macular edema? : Comment on: Gao BB et al. Extracellular carbonic anhydrase mediates hemorrhagic retinal and cerebral vascular permeability through prekallikrein activation. Nat Med. 2007 Feb;13(2):181-8.
Recently, Gao et al. published an experimental study based on the pathophysiology of diabetic macular edema in Nature Medicine (Nat Med. 2007 Feb;13(2):181-8). They found an increased amount of carbonic anhydrase in the vitreous, which causes a pH shift. This activates the kallikrein-kinin system and leads to increased retinal vascular permeability. In this comment the clinical implications of this article are discussed.
Zeitz
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Klinik und Poliklinik für Augenheilkunde, Universitätklinikum Hamburg-Eppendorf, Martinitsr. 52, Hamburg 20246, Germany. zeitz@uke.uni-hamburg.de
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D002199:Capillary Permeability; D002256:Carbonic Anhydrases / Q000502:physiology*; D003930:Diabetic Retinopathy / Q000188:drug therapy* / Q000209:etiology* / Q000503:physiopathology; D006801:Humans; D006863:Hydrogen-Ion Concentration; D016234:Kallikrein-Kinin System / Q000502:physiology*; D008269:Macular Edema / Q000188:drug therapy* / Q000209:etiology* / Q000503:physiopathology; D012171:Retinal Vessels / Q000502:physiology; D014822:Vitreous Body / Q000201:enzymology*