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Extensive crosstalk between apoptosis and necroptosis is well-documented and is mediated primarily by the caspase-8 status (pro-apoptotic, anti-necroptotic), post-translational modifications of RIPK1, RIPK3 and MLKL (phosphorylation and ubiquitination), features of ROS signaling, etc [129, 130]

Iron is also integral to enzymes associated with ferroptosis, with lipoxygenases (LOXs) utilizing Fe 2+ as a cofactor to catalyze PUFA peroxidation [33]

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Crosstalk Between LXR and Caveolin-1 Signaling Supports Cholesterol Efflux and Anti-Inflammatory Pathways in Macrophages

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