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More efficient penetration has been shown through directly comparing GSH to a GSH monoethyl ester (GEE), showing that GEE significantly elevated intracellular GSH levels in mesencephalic cultures (Zeevalk et al., 2007)

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Thus, GPX4 is the main defender of cellular ferroptosis in living organisms [95, 96]

A significant reduction in total mitochondrial BAX, comprising loosely attached and inserted forms, was observed following B-017 treatment (Fig

Gegen-Qinlian decoction alleviates metabolic dysfunction-associated steatohepatitis by modulating the microbiota-bile acid axis in mice

Since the discovery of FSP1, more and more GPX4-independent ferroptosis pathways have been discovered in various physiological and pathological processes Drugs targeting GPX4-independent ferroptosis pathway may become a new direction for the treatment of diseases