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Early correction of energy metabolic reprogramming in TECs, along with the restoration of mitochondrial function, is considered a potentially valuable therapeutic approach to reduce the severity and long-term consequences of AKI ( This review outlines the metabolic transitions observed during AKI, emphasizing the underlying pathophysiological mechanisms and key regulatory pathways implicated in mitochondrial dysfunction and energy metabolism
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151 For the NADPH-synthesis enzymes involved in anapleurotic reactions, including IDH1/2, ME1/2/3, and CPT1/2, the targeting inhibitors are also being extensively developed
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