Reactive Oxygen Species, SUMOylation, and Endothelial Inflammation. (6th September 2012)

• Record Type: Journal Article
• Authors: Le, Nhat-Tu; Corsetti, James P.; Dehoff-Sparks, Janet L.; Sparks, Charles E.; Fujiwara, Keigi; Abe, Jun-ichi
• Other Names: Aikawa Masanori Academic Editor.
• Is Part Of: International journal of inflammation. Volume 2012(2012)
• Publication Date: 2012-09-06
• Subjects: Inflammation -- Periodicals; Inflammation; Inflammation; Periodicals; 617.22
• DOI: 10.1155/2012/678190
• Languages: English
• ISSNs: 2090-8040

Abstract

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.