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Employing gene editing techniques alongside both in vivo and in vitro experiments, we provide novel evidence that the dysfunction of SLC25A39-mediated mitochondrial import of GSH constitutes a pathological alteration following TBI, leading to mitochondrial dysfunction and subsequent initiation of oxidative stress and neuronal cell death

It has been widely used in preclinical therapy for tumors, intestinal diseases, and anemia via oral administration 20,21,22

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An online research listing does not mean that the product has undergone an MHRA assessment of quality, safety and efficacy

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