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In the midst of hype over the new armamentarium in the war against retinal neovascularisation, typified by Lucentis and Macugen, many have lost sight (no pun) of the grail of retinal disease treatment. This has ever been to actively regress existing pathological vasculature, a preimary cause of vision loss in dieases such as 'wet' age-related macular degeneration, diabetic retinopathy, neovascular glaucoma and others.
In a clear stride toward this goal, Pierre Hardy and coworkers at the McGill University, Montreal, Canada have published an elegant study showing that activation of CD36 inhibits and induces regression of inflammatory corneal neovascularisation (CNV). Using a murine model of inflammatory CNV, CD36 expression was found to be upregulated after corneal injury; it's expression being limited to the corneal epithelium, limbus and invading microvasculature. Blocking CD36 actrivation with FA6-152, an anti-CD36 monoclonal against the thrombospondin binding site, significantly increased CNV. Conversely, activating CD36 with POVPC (a phosphatidylcholine ligand of CD26) dose-dependantly inhibited CNV. This ligand also caused regression of the existing CNV by ~ 75%. The authors conclude the CD36 is involved both physiologically and pharmacologically in the inhibition and regression of CNV. This author is anxious to find out with the retinal pigment epithelium (which also expresses CD36) will respond to receptor activation in an equivalent manner.
Message posted by: Simon Chandler
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