Tumor Necrosis Factor-α Modulates Cerebral Aneurysm Formation and Rupture

Overview

Journal Transl Stroke Res

Publisher Springer

Date 2013 Dec 11

PMID 24323710

Citations 34

Authors

Robert M Starke

Daniel M S Raper

Dale Ding

Nohra Chalouhi

Gary K Owens

David M Hasan

Ricky Medel

Aaron S Dumont

Affiliations

Soon will be listed here.

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.

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