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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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Wound healing activity of carbon monoxide liberated from co-releasing molecule (CO-RM)