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The conversion of fatty acids to acyl-coenzyme A (CoA) esters is a crucial regulatory step in ferroptosis [14,15,16]

These effects appeared complex and context-dependent, varying with dose, timing, and baseline endocrine status

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Evolving theories of the pathophysiology of major depression have implicated overactivation of inflammatory pathways, ill-defined changes in glutamate metabolism, and disconnection of cortical and subcortical components of a neural reward circuit

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