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Loss of intracellular GSH is likely multifactorial and includes generation of high levels of hydroperoxy-phospholipids (which directly or indirectly oxidize GSH and limit GSSG recycling by reductases) as well as active export of GSSG generated by high GPX4 activity (7, 8, 21)

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Notably, metabolites such as AGEs, dysregulated ketone bodies, and BCAAs have been demonstrated to be directly or indirectly associated with structural abnormalities and functional decline in the lung (e.g., impaired surfactant synthesis, diminished respiratory muscle function)