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In the DVT mouse model, endothelial activation and platelet function were stimulated by LPS but not by PAD4 deficiency, and PAD4 -/- mice formed NETs-free thrombi

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These ROS, reach the brain via the circulation, disrupting neuronal antioxidant defenses, inducing lipid peroxidation and protein modification, and promoting the accumulation of the lipid peroxidation end product 4-HNE to cause astrocytic ferroptosis and ultimately lead to synaptic structural degeneration and memory deficits [341,342,343]

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