Abstract
An increasing body of evidence suggests that different genetic factors, such as angiotensin-converting enzyme (ACE) I/D , angiotensin II type-1 receptor (AT1R) A1166C, methylenetetrahydrofolate reductase (MTHFR) C677T and ENOS G894T variants are associated with an endothelial dysfunction (ED). EDs are relatively new phenomena that are presumed to contribute to vasoregulatory malfunctions at the small-vessel level. Ever more clinical observations indicate that the above genetic variants are also associated with cerebral small-vessel disorders. This article reviews the knowledge available on the roles of ED- associated genetic variants in cerebral circulatory disorders, and suggests that EDs can be causative factors for different common cerebral pathologies such as leukoaraiosis or/and small-vessel infarcts. Newly-developed drugs involving phosphodiesterase type-5 inhibitors, which improve the endothelial functions, may comprise a new approach to the treatment and prevention of small-vessel cerebral circulatory disorders.
Keywords: Leukoaraiosis, small-vessel infarcts, endothelial dysfunction, nitric oxide, endothelin-1, MTHFR C677T, angiotensin-converting enzyme I/D, ENOS G894T, AT1R A1166C, genetic variant
Mini-Reviews in Medicinal Chemistry
Title: Genetic Variant-Associated Endothelial Dysfunction Behind Small-Vessel Cerebral Circulatory Disorders: A New Pathomechanism Behind Common Cerebral Phenotypes
Volume: 7 Issue: 5
Author(s): Zoltan Szolnoki
Affiliation:
Keywords: Leukoaraiosis, small-vessel infarcts, endothelial dysfunction, nitric oxide, endothelin-1, MTHFR C677T, angiotensin-converting enzyme I/D, ENOS G894T, AT1R A1166C, genetic variant
Abstract: An increasing body of evidence suggests that different genetic factors, such as angiotensin-converting enzyme (ACE) I/D , angiotensin II type-1 receptor (AT1R) A1166C, methylenetetrahydrofolate reductase (MTHFR) C677T and ENOS G894T variants are associated with an endothelial dysfunction (ED). EDs are relatively new phenomena that are presumed to contribute to vasoregulatory malfunctions at the small-vessel level. Ever more clinical observations indicate that the above genetic variants are also associated with cerebral small-vessel disorders. This article reviews the knowledge available on the roles of ED- associated genetic variants in cerebral circulatory disorders, and suggests that EDs can be causative factors for different common cerebral pathologies such as leukoaraiosis or/and small-vessel infarcts. Newly-developed drugs involving phosphodiesterase type-5 inhibitors, which improve the endothelial functions, may comprise a new approach to the treatment and prevention of small-vessel cerebral circulatory disorders.
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Cite this article as:
Szolnoki Zoltan, Genetic Variant-Associated Endothelial Dysfunction Behind Small-Vessel Cerebral Circulatory Disorders: A New Pathomechanism Behind Common Cerebral Phenotypes, Mini-Reviews in Medicinal Chemistry 2007; 7 (5) . https://dx.doi.org/10.2174/138955707780619572
DOI https://dx.doi.org/10.2174/138955707780619572 |
Print ISSN 1389-5575 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5607 |
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