Hyperhomocysteinemia And Pathogenetic Mechanisms Of Ischemic Stroke

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Makhmudovich , A. M. ., Sattarovna, R. G. ., Maksudovna, V. N. . ., & Azamatovich, J. S. . . (2021). Hyperhomocysteinemia And Pathogenetic Mechanisms Of Ischemic Stroke. The American Journal of Medical Sciences and Pharmaceutical Research, 3(02), 66–76. https://doi.org/10.37547/TAJMSPR/Volume03Issue02-10
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Abstract

The article is intended to give basic information and the role of homocysteine in the human body. The amino acid homocysteine is a product of methionine demethylation. When the level of homocysteine increases, it damages the tissue structures of the arteries, initiating the release of cytokines, cyclins and other inflammatory mediators. Its accumulation leads to loosening of the arterial walls, the formation of local defects in the endothelium, which, in turn, leads to the deposition of cholesterol and calcium on the vascular wall. Hyperhomocysteinemia as a consequence of impaired homocysteine metabolism is considered an independent risk factor for stroke in humans. The role of neuroprotective therapy in interrupting or slowing down the sequence of damaging biochemical and molecular processes that can cause irreversible ischemic brain damage is shown.

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