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Specifically, long-term hyperglycemia impairs the function of smooth muscles in the corpus cavernosum by reducing mitochondrial biogenesis, increasing adenosine diphosphate (ADP)/ATP ratios, altering ultra structural changes, and triggering ROS [53]

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This metabolic vulnerability has been exploited as therapeutic modality where depletion of NAD+ using small molecule inhibitors targeting the salvage NAD+ synthesis enzyme nicotinamide phosphoribosyl transferase resulted in strikingly selective cytotoxicity in IDH1 mutant cancer cells [148]

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