Endothelial Dysfunction and Hyperhomocysteinemia-Linked Cerebral Small Vessel Disease: Underlying Mechanisms and Treatment Timing

Cerebral small vessel disease (cSVD)—a common cause of stroke and vascular dementia—is a group of clinical syndromes that affects the brain's small vessels, including arterioles, capillaries, and venules. Its pathogenesis is not fully understood, and effective treatments are limited. Increasing...

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Autores principales:	Shuang Li, Guangjian Li, Xia Luo, Yan Huang, Lan Wen, Jinglun Li
Formato:	article
Lenguaje:	EN
Publicado:	Frontiers Media S.A. 2021
Materias:	cerebral small vessel disease homocysteine hyperhomocysteinemia endothelial dysfunction homocysteine-lowering therapy Neurology. Diseases of the nervous system RC346-429
Acceso en línea:	https://doaj.org/article/b20865aff97049279e28fef7123acf68
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spelling	oai:doaj.org-article:b20865aff97049279e28fef7123acf682021-11-30T16:04:37ZEndothelial Dysfunction and Hyperhomocysteinemia-Linked Cerebral Small Vessel Disease: Underlying Mechanisms and Treatment Timing1664-229510.3389/fneur.2021.736309https://doaj.org/article/b20865aff97049279e28fef7123acf682021-11-01T00:00:00Zhttps://www.frontiersin.org/articles/10.3389/fneur.2021.736309/fullhttps://doaj.org/toc/1664-2295Cerebral small vessel disease (cSVD)—a common cause of stroke and vascular dementia—is a group of clinical syndromes that affects the brain's small vessels, including arterioles, capillaries, and venules. Its pathogenesis is not fully understood, and effective treatments are limited. Increasing evidence indicates that an elevated total serum homocysteine level is directly and indirectly associated with cSVD, and endothelial dysfunction plays an active role in this association. Hyperhomocysteinemia affects endothelial function through oxidative stress, inflammatory pathways, and epigenetic alterations at an early stage, even before the onset of small vessel injuries and the disease. Therefore, hyperhomocysteinemia is potentially an important therapeutic target for cSVD. However, decreasing the homocysteine level is not sufficiently effective, possibly due to delayed treatment, which underlying reason remains unclear. In this review, we examined endothelial dysfunction to understand the close relationship between hyperhomocysteinemia and cSVD and identify the optimal timing for the therapy.Shuang LiShuang LiGuangjian LiXia LuoXia LuoYan HuangYan HuangLan WenJinglun LiJinglun LiFrontiers Media S.A.articlecerebral small vessel diseasehomocysteinehyperhomocysteinemiaendothelial dysfunctionhomocysteine-lowering therapyNeurology. Diseases of the nervous systemRC346-429ENFrontiers in Neurology, Vol 12 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	cerebral small vessel disease homocysteine hyperhomocysteinemia endothelial dysfunction homocysteine-lowering therapy Neurology. Diseases of the nervous system RC346-429
spellingShingle	cerebral small vessel disease homocysteine hyperhomocysteinemia endothelial dysfunction homocysteine-lowering therapy Neurology. Diseases of the nervous system RC346-429 Shuang Li Shuang Li Guangjian Li Xia Luo Xia Luo Yan Huang Yan Huang Lan Wen Jinglun Li Jinglun Li Endothelial Dysfunction and Hyperhomocysteinemia-Linked Cerebral Small Vessel Disease: Underlying Mechanisms and Treatment Timing
description	Cerebral small vessel disease (cSVD)—a common cause of stroke and vascular dementia—is a group of clinical syndromes that affects the brain's small vessels, including arterioles, capillaries, and venules. Its pathogenesis is not fully understood, and effective treatments are limited. Increasing evidence indicates that an elevated total serum homocysteine level is directly and indirectly associated with cSVD, and endothelial dysfunction plays an active role in this association. Hyperhomocysteinemia affects endothelial function through oxidative stress, inflammatory pathways, and epigenetic alterations at an early stage, even before the onset of small vessel injuries and the disease. Therefore, hyperhomocysteinemia is potentially an important therapeutic target for cSVD. However, decreasing the homocysteine level is not sufficiently effective, possibly due to delayed treatment, which underlying reason remains unclear. In this review, we examined endothelial dysfunction to understand the close relationship between hyperhomocysteinemia and cSVD and identify the optimal timing for the therapy.
format	article
author	Shuang Li Shuang Li Guangjian Li Xia Luo Xia Luo Yan Huang Yan Huang Lan Wen Jinglun Li Jinglun Li
author_facet	Shuang Li Shuang Li Guangjian Li Xia Luo Xia Luo Yan Huang Yan Huang Lan Wen Jinglun Li Jinglun Li
author_sort	Shuang Li
title	Endothelial Dysfunction and Hyperhomocysteinemia-Linked Cerebral Small Vessel Disease: Underlying Mechanisms and Treatment Timing
title_short	Endothelial Dysfunction and Hyperhomocysteinemia-Linked Cerebral Small Vessel Disease: Underlying Mechanisms and Treatment Timing
title_full	Endothelial Dysfunction and Hyperhomocysteinemia-Linked Cerebral Small Vessel Disease: Underlying Mechanisms and Treatment Timing
title_fullStr	Endothelial Dysfunction and Hyperhomocysteinemia-Linked Cerebral Small Vessel Disease: Underlying Mechanisms and Treatment Timing
title_full_unstemmed	Endothelial Dysfunction and Hyperhomocysteinemia-Linked Cerebral Small Vessel Disease: Underlying Mechanisms and Treatment Timing
title_sort	endothelial dysfunction and hyperhomocysteinemia-linked cerebral small vessel disease: underlying mechanisms and treatment timing
publisher	Frontiers Media S.A.
publishDate	2021
url	https://doaj.org/article/b20865aff97049279e28fef7123acf68
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Endothelial Dysfunction and Hyperhomocysteinemia-Linked Cerebral Small Vessel Disease: Underlying Mechanisms and Treatment Timing

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