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The transient receptor potential channel TRPM4 has been shown to promote ox-LDL-induced dysfunction in HCAECs through ferroptosis mechanisms (33)

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The flux of cysteine and the end products are driven by how much methionine is eaten, as well as how much glutathione is needed to combat oxidative stress in cells.[ref][ref] Homocysteine thiolactone: Damaging endothelial cells, increasing inflammation Homocysteine can also become homocysteine thiolactone when a thiol group is attached