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Müller glial dysfunction during diabetic retinopathy in rats is reduced by the acrolein-scavenging drug, 2-hydrazino-4,6-dimethylpyrimidine – published online 15/08/2018

Fig from Muller paper

Rosemary E. McDowell, Peter Barabas, Josy Augustine, Olivier Chevallier, Philip McCarron, Mei Chen, J. Graham McGeown, Tim M. Curtis

Müller cells play a critical role in maintaining retinal function and survival. These cells are particularly vulnerable to damage in diabetes and their dysfunction has been linked to the pathogenesis of diabetic retinopathy. Up to now, the mechanisms through which diabetes affects these cells has remained unclear. In this issue, McDowell et al (https://doi.org/10.1007/s00125-018-4707-y) report that accumulation of the acrolein-derived advanced lipoxidation end-product, Nε-(3-formyl-3,4-dehydropiperidino)lysine (FDP-lysine), on Müller cell proteins contributes to the dysfunction of these cells during diabetes. They identify a new drug called 2-hydrazino-4,6-dimethylpyrimidine (2-HDP) as a potent acrolein scavenger and demonstrate that this compound prevents Müller cell FDP-lysine accumulation and dysfunction in the retina in vivo, in rat models of diabetes. This drug also reduced oxidative and inflammatory responses in the retina and improved neuroretinal function during experimental diabetes. These findings suggest that acrolein scavenging may represent a novel therapeutic approach for the early-stage treatment of diabetic retinopathy.

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