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. 2020 Sep 16;10(9):637.
doi: 10.3390/brainsci10090637.

Hyperhomocysteinemia and Endothelial Dysfunction in Multiple Sclerosis

Ekaterina Dubchenko  1   2 , Alexander Ivanov  3 , Natalia Spirina  4 , Nina Smirnova  1   5 , Mikhail Melnikov  1   5   6 , Alexey Boyko  1   5 , Evgeniy Gusev  5 , Aslan Kubatiev  3
Affiliations

Hyperhomocysteinemia and Endothelial Dysfunction in Multiple Sclerosis

Ekaterina Dubchenko et al. Brain Sci. .

Abstract

Endothelial dysfunction is recognized as one of the leading factors in the pathogenesis of diseases of the central nervous system of various etiologies. Numerous studies have shown the role of hyperhomocysteinemia in the development of endothelial dysfunction and the prothrombogenic state. The most important condition in the development of multiple sclerosis (MS) is a dysregulation of the blood-brain barrier (BBB) and transendothelial leukocyte migration. It has been proven that homocysteine also contributes to the damage of neurons by the mechanism of excitotoxicity and the induction of the apoptosis of neurons. These processes can be one of the factors of neurodegenerative brain damage, which plays a leading role in the progression of MS. This review describes the pleiotropic effect of homocysteine on these processes and its role in MS pathogenesis.

Keywords: endothelial dysfunction; homocysteine; hyperhomocysteinemia; multiple sclerosis.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Homocysteine metabolism pathway (adapted from Esse et al., 2019 [19]).
Figure 2
Figure 2
The possible mechanism action of homocysteine in multiple sclerosis pathogenesis: (i) oxidative stress; (ii) inflammation (upregulation of adhesion molecule expression, T-cell activation, inducing pro-inflammatory cytokine production).
See this image and copyright information in PMC

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