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AMSC-based cell therapy alleviate APAP-induced hepatotoxicity by enhancing mitochondrial biogenesis and mitophagy In the previous study, we found that AMSCs treatment can improve mitochondrial function by reducing JNK activation, but the underlying mechanism is unclear [23]

Trimethylamine n-oxide impairs pyruvate and fatty acid oxidation in cardiac mitochondria

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Although MTX caused an insignificant rise in CARN compared with control, in carnitine-depleted MD-treated rats, MTX caused a progressive decrease in serum total and free carnitine