title: Tumor necrosis factor-α modulates cerebral aneurysm formation and rupture.
abstract: 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.
authors: Department of Neurological Surgery, University of Virginia, Charlottesville, VA, USA.
authors: Robert M
authors: RM
authors: Starke
authors: Daniel M S
authors: DM
authors: Raper
authors: Dale
authors: D
authors: Ding
authors: Nohra
authors: N
authors: Chalouhi
authors: Gary K
authors: GK
authors: Owens
authors: David M
authors: DM
authors: Hasan
authors: Ricky
authors: R
authors: Medel
authors: Aaron S
authors: AS
authors: Dumont
mesh_terms: D017542:Aneurysm, Ruptured / Q000378:metabolism*; D000818:Animals; D004195:Disease Models, Animal; D006801:Humans; D007249:Inflammation / Q000378:metabolism; D002532:Intracranial Aneurysm / Q000378:metabolism*; D018384:Oxidative Stress; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism*
chemical_list: D014409:Tumor Necrosis Factor-alpha