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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

Free Radic Biol Med 63:5164 Schrammel A, Gorren AC, Schmidt K, Pfeiffer S, Mayer B (2003) S-nitrosation of glutathione by nitric oxide, peroxynitrite, and (*)NO/O(2)(*-)

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Besides, protein undergoes carbonylation, another form of protein oxidative modification in which ROS groups bind to specific amino acids, affecting protein stability and activity ( Furthermore, ROS/RNS can directly attack DNA, causing oxidative DNA damage in IBD ( 2.3 Mitochondrial dysfunction Mitochondria, with their functions in energy production, calcium homeostasis, and membrane excitability, are thought to substantially impact the pathology of IBD, as their dysfunction may initiate and advance the disease