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Consistently, knockout of LPCAT3 in lung epithelial cells conferred resistance to ferroptosis induced by the Ras-selective lethal compound 3 (RSL3), and reduced expression of ACSL4 or LPCAT3 diminished the availability of peroxidizable phospholipid substrates [39], thereby inhibiting ferroptosis and further emphasizing the critical role of PUFA metabolism in ferroptosis

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