Joseph and Marie Field Cerebrovascular Research Laboratory, Division of Neurovascular & Endovascular Surgery, Department of Neurological Surgery, Thomas Jefferson University, Philadelphia, PA 19107, USA.
Mediators Inflamm. 2012;2012:271582. doi: 10.1155/2012/271582. Epub 2012 Dec 13.
Smoking is an established risk factor for subarachnoid hemorrhage yet the underlying mechanisms are largely unknown. Recent data has implicated a role of inflammation in the development of cerebral aneurysms. Inflammation accompanying cigarette smoke exposure may thus be a critical pathway underlying the development, progression, and rupture of cerebral aneurysms. Various constituents of the inflammatory response appear to be involved including adhesion molecules, cytokines, reactive oxygen species, leukocytes, matrix metalloproteinases, and vascular smooth muscle cells. Characterization of the molecular basis of the inflammatory response accompanying cigarette smoke exposure will provide a rational approach for future targeted therapy. In this paper, we review the current body of knowledge implicating cigarette smoke-induced inflammation in cerebral aneurysm formation/rupture and attempt to highlight important avenues for future investigation.
吸烟是蛛网膜下腔出血的既定危险因素,但其中的潜在机制在很大程度上尚不清楚。最近的数据表明,炎症在脑动脉瘤的发展中起作用。因此,伴随香烟烟雾暴露的炎症可能是脑动脉瘤的发展、进展和破裂的关键途径。炎症反应的各种成分似乎都参与其中,包括黏附分子、细胞因子、活性氧、白细胞、基质金属蛋白酶和血管平滑肌细胞。描述伴随香烟烟雾暴露的炎症反应的分子基础将为未来的靶向治疗提供合理的方法。在本文中,我们回顾了目前的知识体系,这些知识表明香烟烟雾引起的炎症与脑动脉瘤的形成/破裂有关,并试图强调未来研究的重要途径。