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Specific disulfide linkage between homocysteine and the sulfhydryl group of an intracellular protein may be an alternative molecular mechanism underlying hyperhomocysteinemia-induced vascular dysfunction

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It plays a central role in neutralizing free radicals, supporting liver detoxification, and maintaining immune function

For example, ER stress activates DNA damage inducible transcript 3 (DDIT3, also known as CHOP)- and mitogen-activated protein kinase 8 (MAPK8, also known as JNK)-dependent apoptosis pathways, whereas heat shock protein family A member 5 (HSPA5, also known as BIP) SSG at Cys420/441 modulates ATPase activity and protein folding, paradoxically suppressing apoptosis 49