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Consequently, it can be deduced that each branch of Gln metabolism appears to be critical for NKT cellular homeostasis and mitochondrial function

It was reported that it could raise intracellular GSH by increasing SLC7A11 expression, efficiently leading to GPX4 enhancement and ferroptosis suppression in the ISO-induced injury model of H9C2 cells and rat myocardium [49]

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In renal epithelial cell cultures, studies show the peptide decreases expression of aging-associated markers including p16, p21, and p53proteins that regulate cell cycle arrest and senescence pathways