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ROS-mediated oxidative stress promotes mitochondrial dysfunction, fostering a self-reinforcing cycle where increased ROS generation perpetuates lipids, proteins and DNA oxidation, thereby exacerbating cellular injury [231]

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In diet-induced obesity animal models, NNMT inhibition demonstrated metabolic changes including alterations in adipocyte lipid content without affecting food intake patterns, coupled with significant reductions in white adipose tissue mass in treated mice

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