Role of oxidative stress in the pathogenesis of abdominal aortic aneurysms

Michael L. McCormick, Dan Gavrila, Neal L. Weintraub

Research output: Contribution to journalReview article

210 Scopus citations

Abstract

The role of inflammation in the pathogenesis of abdominal aortic aneurysms (AAA) is well established. The inflammatory process leads to protease-mediated degradation of the extracellular matrix and apoptosis of smooth muscle cells (SMC), which are the predominant matrix synthesizing cells of the vascular wall. These processes act in concert to progressively weaken the aortic wall, resulting in dilatation and aneurysm formation. Oxidative stress is invariably increased in, and contributes importantly to, the pathophysiology of inflammation. Moreover, reactive oxygen species (ROS) play a key role in regulation of matrix metalloproteinases and induction of SMC apoptosis. ROS may also contribute to the pathogenesis of hypertension, a risk factor for AAA. Emerging evidence suggests that ROS and reactive nitrogen species (RNS) are associated with AAA formation in animal models and in humans. Although experimental data are limited, several studies suggest that modulation of ROS production or activity may suppress AAA formation and improve experimental outcome in rodent models. Although a number of enzymes can produce injurious ROS in the vasculature, increasing evidence points toward a role for NADPH oxidase as a source of oxidative stress in the pathogenesis of AAA.

Original languageEnglish (US)
Pages (from-to)461-469
Number of pages9
JournalArteriosclerosis, thrombosis, and vascular biology
Volume27
Issue number3
DOIs
StatePublished - Mar 1 2007

    Fingerprint

Keywords

  • Aneurysm
  • Inflammation
  • NADPH oxidase
  • Oxidative stress
  • Reactive oxygen species

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this