Abstract
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.
Highlights
Cigarette smoking is a major health hazard, with 5.4 million premature deaths worldwide every year and an average loss of 13 to 15 years of life expectancy [1]
We found that Cigarette smoke (CS) directly produced marked phenotypic modulation with decreased expression of vascular smooth muscle cells (VSMC) marker genes and myocardin while markedly increasing expression of inflammatory/matrix remodeling genes (MMP, MCP-1, IL-1, and tumor necrosis factor-α (TNF-α) expression)
Many of the abnormalities observed in cerebral aneurysm including endothelial dysfunction, proinflammatory reactions, adhesion molecule expression, VSMC proliferation, apoptosis, matrix metalloproteinases (MMP) activation, and tissue destruction may be at least partly explained by the effects of increased oxidative stress [8, 45, 140,141,142]
Summary
Cigarette smoking is a major health hazard, with 5.4 million premature deaths worldwide every year and an average loss of 13 to 15 years of life expectancy [1]. Cigarette smoke (CS) is the most significant modifiable risk factor for cerebral aneurysm formation. A burgeoning but currently incomplete body of evidence suggests that vascular inflammation, a key component of cerebral aneurysm pathogenesis, may provide the common link between cigarette smoking and aneurysm formation and rupture. Exposure to chemicals in cigarette smoke has consistently been shown to have a significant effect on various pathways of the immune/inflammatory response in the cerebrovascular system [6, 7]. This complex interplay between CS and vascular inflammation in cerebral aneurysm pathogenesis may represent an important target for future. The present discussion critically evaluates the existing body of literature implicating active and passive cigarette smoking in aneurysm formation/rupture and attempts to highlight important avenues for future investigation
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