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59 These findings suggest that vesicle-mediated signaling may either amplify or restrain ferroptosis depending on cargo composition and uptake efficiency, highlighting extracellular vesicles as bidirectional regulators of ferroptotic susceptibility rather than unidirectional death signals

The long-term effects of GP1 medications are still being studied

[47] reported similar findings, showing that the AMPK activator metformin increased LDLR expression in HepG2 cells through both SREBP-2-dependent and independent mechanisms

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