Starke Robert M, Raper Daniel M S, Ding Dale, Chalouhi Nohra, Owens Gary K, Hasan David M, Medel Ricky, Dumont Aaron S
Department of Neurological Surgery, University of Virginia, Charlottesville, VA, USA.
Transl Stroke Res. 2014 Apr;5(2):269-77. doi: 10.1007/s12975-013-0287-9. Epub 2013 Sep 20.
Inflammation is a critical process behind cerebral aneurysm formation and rupture. Tumor necrosis factor alpha (TNF-α) is a key immune modulator that has been implicated in cerebral aneurysm pathophysiology. This may occur through TNF-α-mediated endothelial injury, smooth muscle cell phenotypic modulation, recruitment of macrophages, activation of chemotactic cytokines, upregulation of matrix remodeling genes, production of free radicals leading to oxidative stress, and ultimately cellular apoptosis. Recent studies have indicated that TNF-α may be a potential target for the development of novel medical therapies, but additional experimental data is needed to clarify the intricacies of TNF-α activation and its critical downstream targets in cerebral aneurysms. This review provides an update on the mechanisms underlying TNF-α-induced molecular modulation in cerebral aneurysms.
炎症是脑动脉瘤形成和破裂背后的关键过程。肿瘤坏死因子α（TNF-α）是一种关键的免疫调节剂，已被认为与脑动脉瘤的病理生理学有关。这可能通过TNF-α介导的内皮损伤、平滑肌细胞表型调节、巨噬细胞募集、趋化细胞因子激活、基质重塑基因上调、导致氧化应激的自由基产生以及最终的细胞凋亡而发生。最近的研究表明，TNF-α可能是新型药物治疗开发的潜在靶点，但需要更多的实验数据来阐明TNF-α激活及其在脑动脉瘤中的关键下游靶点的复杂性。本综述提供了关于TNF-α诱导脑动脉瘤分子调节的潜在机制的最新信息。
