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(2022) 66:e2200174

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Studies tracking radiolabeled peptide demonstrate metabolism primarily in plasma, with resulting amino acids entering normal metabolic pathways

We found that CPT1B suppression related FA metabolic dysfunction is a mechanism of UA induced cardiomyocytic injury and could be rescued by exogenous LC

Over time and with increasing OS, mechanisms that promote GSH synthesis may become overwhelmed, leading to decreased GSH levels as GSH is consumed in oxidation and insufficiently replaced