The Role of Oxidative Stress in Cerebral Aneurysm Formation and Rupture

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.

Review of Cerebral Aneurysm Formation, Growth, and Rupture

“…29 Aoki et al 30 showed that ROSproducing genes were upregulated, and that ROS-eliminating genes were suppressed in CAs in mice, which indicated that overproduction of ROS occurred in aneurysm walls. Moreover, both a free radical scavenger (edaravone) and the deletion of ROS-producing gene (p47phox) effectively inhibited CA formation by suppressing inflammation in aneurysmal walls.…”

“…Moreover, both a free radical scavenger (edaravone) and the deletion of ROS-producing gene (p47phox) effectively inhibited CA formation by suppressing inflammation in aneurysmal walls. In a critical review of the literature on ROS, Starke et al 29 found that oxidative stress can induce important processes leading to CA formation including direct endothelial injury, SMC phenotypic modulation and apoptosis, recruitment and invasion of inflammatory cells through upregulation of chemotactic cytokines and adhesion molecules, and MMPs activation.…”

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“…A mortalidade após HSA pode ser acima de 50%, e daqueles que sobrevivem, apenas 30-45% retornam aos seus empregos anteriores, e até 30% permanecem incapacitados. Os mecanismos exatos por trás da formação e ruptura do aneurisma não são claros, mas a inflamação e a degeneração tecidual são elementos-chave 7 .…”

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