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Depletion of GSH or inactivation of GPX4 leads to LOOH accumulation, resulting in the buildup of toxic peroxidation products, consequent membrane damage, and cell death (29)

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Nucl Recept Signal

Because typical early atherosclerotic lesion formation observed in hyperhomocysteinemic animals can be prevented by an antiplatelet therapy with dipyridamole, the authors concluded that platelet-mediated proliferation of smooth muscle cells is a potential cellular mechanism involved in the atherogenicity of hyperhomocysteinemia