Abstract
Although the exact mechanism through which NADPH oxidases (Nox's) generate reactive oxygen species (ROS) is still not completely understood, it is widely considered that ROS accumulation is the cause of oxidative stress in endothelial cells. Increasing pieces of evidence strongly indicate the role for ROS in endothelial inflammation and dysfunction and subsequent development of atherosclerotic plaques, which are causes of various pathological cardiac events. An overview for a causative relationship between ROS and endothelial inflammation will be provided in this review. Particularly, a crucial role for specific protein SUMOylation in endothelial inflammation will be presented. Given that SUMOylation of specific proteins leads to increased endothelial inflammation, targeting specific SUMOylated proteins may be an elegant, effective strategy to control inflammation. In addition, the involvement of ROS production in increasing the risk of recurrent coronary events in a sub-group of non-diabetic, post-infarction patients with elevated levels of HDL-cholesterol will be presented with the emphasis that elevated HDL-cholesterol under certain inflammatory conditions can lead to increased incidence of cardiovascular events.
Original language | English (US) |
---|---|
Article number | 678190 |
Journal | International Journal of Inflammation |
Volume | 2012 |
DOIs | |
State | Published - Nov 7 2012 |
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ASJC Scopus subject areas
- Immunology and Allergy
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Reactive oxygen species, SUMOylation, and endothelial inflammation. / Le, Nhat Tu; Corsetti, James P.; Dehoff-Sparks, Janet L.; Sparks, Charles E.; Fujiwara, Keigi; Abe, Jun Ichi.
In: International Journal of Inflammation, Vol. 2012, 678190, 07.11.2012.Research output: Contribution to journal › Review article
}
TY - JOUR
T1 - Reactive oxygen species, SUMOylation, and endothelial inflammation
AU - Le, Nhat Tu
AU - Corsetti, James P.
AU - Dehoff-Sparks, Janet L.
AU - Sparks, Charles E.
AU - Fujiwara, Keigi
AU - Abe, Jun Ichi
PY - 2012/11/7
Y1 - 2012/11/7
N2 - Although the exact mechanism through which NADPH oxidases (Nox's) generate reactive oxygen species (ROS) is still not completely understood, it is widely considered that ROS accumulation is the cause of oxidative stress in endothelial cells. Increasing pieces of evidence strongly indicate the role for ROS in endothelial inflammation and dysfunction and subsequent development of atherosclerotic plaques, which are causes of various pathological cardiac events. An overview for a causative relationship between ROS and endothelial inflammation will be provided in this review. Particularly, a crucial role for specific protein SUMOylation in endothelial inflammation will be presented. Given that SUMOylation of specific proteins leads to increased endothelial inflammation, targeting specific SUMOylated proteins may be an elegant, effective strategy to control inflammation. In addition, the involvement of ROS production in increasing the risk of recurrent coronary events in a sub-group of non-diabetic, post-infarction patients with elevated levels of HDL-cholesterol will be presented with the emphasis that elevated HDL-cholesterol under certain inflammatory conditions can lead to increased incidence of cardiovascular events.
AB - Although the exact mechanism through which NADPH oxidases (Nox's) generate reactive oxygen species (ROS) is still not completely understood, it is widely considered that ROS accumulation is the cause of oxidative stress in endothelial cells. Increasing pieces of evidence strongly indicate the role for ROS in endothelial inflammation and dysfunction and subsequent development of atherosclerotic plaques, which are causes of various pathological cardiac events. An overview for a causative relationship between ROS and endothelial inflammation will be provided in this review. Particularly, a crucial role for specific protein SUMOylation in endothelial inflammation will be presented. Given that SUMOylation of specific proteins leads to increased endothelial inflammation, targeting specific SUMOylated proteins may be an elegant, effective strategy to control inflammation. In addition, the involvement of ROS production in increasing the risk of recurrent coronary events in a sub-group of non-diabetic, post-infarction patients with elevated levels of HDL-cholesterol will be presented with the emphasis that elevated HDL-cholesterol under certain inflammatory conditions can lead to increased incidence of cardiovascular events.
UR - http://www.scopus.com/inward/record.url?scp=84876511553&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84876511553&partnerID=8YFLogxK
U2 - 10.1155/2012/678190
DO - 10.1155/2012/678190
M3 - Review article
AN - SCOPUS:84876511553
VL - 2012
JO - International Journal of Inflammation
JF - International Journal of Inflammation
SN - 2090-8040
M1 - 678190
ER -