Joseph and Marie Field Cerebrovascular Research Laboratory, Division of Neurovascular & Endovascular Surgery, Department of Neurological Surgery, Thomas Jefferson University and Jefferson Hospital for Neuroscience, Philadelphia, Pennsylvania 19107, USA.
Curr Neurovasc Res. 2013 Aug;10(3):247-55. doi: 10.2174/15672026113109990003.
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.
氧化应激被认为是导致脑血管疾病进展的原因之一。此外，氧化应激可能会增加炎症，而炎症是导致脑动脉瘤发展和破裂的关键因素。氧化应激可诱导导致脑动脉瘤形成的重要过程，包括直接内皮损伤以及平滑肌细胞表型向炎症表型的转变，最终导致细胞凋亡。氧化应激通过上调趋化细胞因子和黏附分子导致募集和浸润炎症细胞。自由基可激活基质金属蛋白酶，导致血管壁重塑和破裂。自由基介导脂质过氧化，导致动脉粥样硬化，并导致血流动力学应激和高血压病理，所有这些都是脑动脉瘤发展的重要组成部分。初步研究表明，针对氧化应激的治疗方法可能为脑动脉瘤的治疗提供未来的有益方法，但需要进一步的研究来确定自由基在脑动脉瘤形成和破裂中的作用。本综述的目的是评估氧化应激在脑动脉瘤发病机制中的作用。
