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 language | English (US) |
|---|---|
| Pages (from-to) | 461-469 |
| Number of pages | 9 |
| Journal | Arteriosclerosis, thrombosis, and vascular biology |
| Volume | 27 |
| Issue number | 3 |
| DOIs | |
| State | Published - Mar 1 2007 |
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Keywords
- Aneurysm
- Inflammation
- NADPH oxidase
- Oxidative stress
- Reactive oxygen species
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine
Cite this
Role of oxidative stress in the pathogenesis of abdominal aortic aneurysms. / McCormick, Michael L.; Gavrila, Dan; Weintraub, Neal Lee.
In: Arteriosclerosis, thrombosis, and vascular biology, Vol. 27, No. 3, 01.03.2007, p. 461-469.Research output: Contribution to journal › Review article
}
TY - JOUR
T1 - Role of oxidative stress in the pathogenesis of abdominal aortic aneurysms
AU - McCormick, Michael L.
AU - Gavrila, Dan
AU - Weintraub, Neal Lee
PY - 2007/3/1
Y1 - 2007/3/1
N2 - 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.
AB - 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.
KW - Aneurysm
KW - Inflammation
KW - NADPH oxidase
KW - Oxidative stress
KW - Reactive oxygen species
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U2 - 10.1161/01.ATV.0000257552.94483.14
DO - 10.1161/01.ATV.0000257552.94483.14
M3 - Review article
VL - 27
SP - 461
EP - 469
JO - Arteriosclerosis, Thrombosis, and Vascular Biology
JF - Arteriosclerosis, Thrombosis, and Vascular Biology
SN - 1079-5642
IS - 3
ER -