Abstract
Oxidative stress is known to contribute to the progression of cerebrovascular disease. Additionally, oxidative stress may be increased by, but also augment inflammation, a key contributor to cerebral aneurysm development and rupture. Oxidative stress can induce important processes leading to cerebral aneurysm formation including direct endothelial injury as well as smooth muscle cell phenotypic switching to an inflammatory phenotype and ultimately apoptosis. Oxidative stress leads to recruitment and invasion of inflammatory cells through upregulation of chemotactic cytokines and adhesion molecules. Matrix metalloproteinases can be activated by free radicals leading to vessel wall remodeling and breakdown. Free radicals mediate lipid peroxidation leading to atherosclerosis and contribute to hemodynamic stress and hypertensive pathology, all integral elements of cerebral aneurysm development. Preliminary studies suggest that therapies targeted at oxidative stress may provide a future beneficial treatment for cerebral aneurysms, but further studies are indicated to define the role of free radicals in cerebral aneurysm formation and rupture. The goal of this review is to assess the role of oxidative stress in cerebral aneurysm pathogenesis.
Keywords: Aneurysm, inflammation, oxidative stress, NADPH oxidase, reactive oxygen species, subarachnoid hemorrhage.
Current Neurovascular Research
Title:The Role of Oxidative Stress in Cerebral Aneurysm Formation and Rupture
Volume: 10 Issue: 3
Author(s): Robert M. Starke, Nohra Chalouhi, Muhammad S. Ali, Pascal M. Jabbour, Stavropoula I. Tjoumakaris, L. Fernando Gonzalez, Robert H. Rosenwasser, Walter J. Koch and Aaron S. Dumont
Affiliation:
Keywords: Aneurysm, inflammation, oxidative stress, NADPH oxidase, reactive oxygen species, subarachnoid hemorrhage.
Abstract: Oxidative stress is known to contribute to the progression of cerebrovascular disease. Additionally, oxidative stress may be increased by, but also augment inflammation, a key contributor to cerebral aneurysm development and rupture. Oxidative stress can induce important processes leading to cerebral aneurysm formation including direct endothelial injury as well as smooth muscle cell phenotypic switching to an inflammatory phenotype and ultimately apoptosis. Oxidative stress leads to recruitment and invasion of inflammatory cells through upregulation of chemotactic cytokines and adhesion molecules. Matrix metalloproteinases can be activated by free radicals leading to vessel wall remodeling and breakdown. Free radicals mediate lipid peroxidation leading to atherosclerosis and contribute to hemodynamic stress and hypertensive pathology, all integral elements of cerebral aneurysm development. Preliminary studies suggest that therapies targeted at oxidative stress may provide a future beneficial treatment for cerebral aneurysms, but further studies are indicated to define the role of free radicals in cerebral aneurysm formation and rupture. The goal of this review is to assess the role of oxidative stress in cerebral aneurysm pathogenesis.
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Cite this article as:
Starke M. Robert, Chalouhi Nohra, Ali S. Muhammad, Jabbour M. Pascal, Tjoumakaris I. Stavropoula, Gonzalez Fernando L., Rosenwasser H. Robert, Koch J. Walter and Dumont S. Aaron, The Role of Oxidative Stress in Cerebral Aneurysm Formation and Rupture, Current Neurovascular Research 2013; 10 (3) . https://dx.doi.org/10.2174/15672026113109990003
DOI https://dx.doi.org/10.2174/15672026113109990003 |
Print ISSN 1567-2026 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5739 |
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