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The pathogenesis of DKD is complex, as it involves extensive damage caused by the reprogramming of mitochondrial metabolism in kidney cells
Free radicals are very unstable and react quickly with other compounds, trying to capture the needed electron to gain stability
In addition, an in vivo study in mice explored the possibility of restricting serine and glycine metabolism for cancer intervention
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Clinical implications of estimated glomerular filtration rate dip following sodiumglucose cotransporter-2 inhibitor initiation on cardiovascular and kidney outcomes
