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The etiology and pathogenesis of preeclampsia are complex and multifactorial, which may be related to an increased inflammatory condition [1], oxidative stress [2], and metabolic dysfunctions [3] at the maternalfetal interface

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Consistently, emerging studies indicated that modulation of oxidative stress, ablation of CD36 (a scavenger receptor known for its function as a fatty acid transporter) (43, 44), or overexpression of GPX4 (44, 45) suppressed lipid peroxidation, restored tumor-infiltrating CD8 + effector functions, and enabled tumor control