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Although additional studies are required to clarify the molecular mechanisms responsible for hyperhomocysteinemia-induced vascular disorders, there is evidence that the direct cytotoxicity of markedly elevated homocysteine and/or of its oxidized by-products (homocysteine thiolactone, homocysteine sulfinic acid, and homocysteic acid) damages endothelial cells (Dudman et al, 1991

The virus enters cells through the interaction of its glycoproteins, gp120 and gp41, with cell surface proteases

Liu CF, Zhou WN, Guo TM, Hou AC, Wei YJ

Comprehending the genetic variations is crucial for enhancing patient compliance and therapeutic success

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10.1016/j.dld.2020.03.020