Tumor Necrosis Factor-α Modulates Cerebral Aneurysm Formation and Rupture

Robert M. Starke, Daniel M.S. Raper, Dale Ding, Nohra Chalouhi, Gary K. Owens, David M. Hasan, Ricky Medel, Aaron S. Dumont

Research output: Contribution to journalArticlepeer-review

55 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)269-277
Number of pages9
JournalTranslational stroke research
Issue number2
StatePublished - Apr 2014
Externally publishedYes


  • Aneurysm
  • Cerebral
  • Inflammation
  • Rupture
  • Subarachnoid hemorrhage
  • TNF- α
  • Tumor necrosis factor

ASJC Scopus subject areas

  • Neuroscience(all)
  • Clinical Neurology
  • Cardiology and Cardiovascular Medicine


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