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As a result, an accumulation of Lipid-OOH occurs: since GSH is the reducing co-substrate of GPX4, able to regulate the redox state of the cell-forming Lipid-OH (Figure 2A), GSH depletion can negatively regulate GPX4, triggering ferroptosis [19]

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Conversely, downregulation of FABP4 by apelin/apelin receptor (APLNR)-mediated Forkhead box O1 (FOXO1) suppression in ECs limits excessive FA transport and tissue accumulation, contributing to atheroprotecton against vascular diseases such as atherosclerosis [86,87,88]

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MEGA-PRESS may be a promising protocol, although the current MEGA-PRESS studies reporting brain GSH in MCI and AD were from a single research group, which may have artificially reduced heterogeneity