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Furthermore, knocking down CBS resulted in a 10-fold induction of a master regulator of EMT, SNAI2 (SLUG) (Supplementary Fig

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

Long-term exposure to the hormone environment can decrease the secretion of derived neurotrophic factor (BDNF) and interfere with neural development (87, 88)

Authors contributions RK is the sole author of the manuscript