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This oxidative milieu incites cellular injury and elicits an inflammatory cascade within the RTCs

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This route however appears to be largely ignored and probably will continue to be ignored, since the strategy so far has been to simply create agonists which are structurally designed to be resistant to DPP-4 (In fact, most modifications to extend the half-life of GLP1R/GIPR/GR agonists so far, do so by making the drugs resistant to DPP-4 )

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