Key result
Angiotensin II contributes to atherogenesis by increasing expression of pro-inflammatory genes and inducing oxidative stress, which activates the NF-κB system.
Angiotensin II contributes to atherogenesis by increasing pro-inflammatory gene expression and inducing oxidative stress, which activates NF-κB.
Cytokines and other inflammatory mediators induce functional changes in the endothelium (“endothelium activation”), which have been shown to be markers of atherosclerotic vascular disease. Endothelial activation accompanies and promotes vascular disease, and is associated with overexpression of chemoattractants and adhesion molecules, which in turn lead to leukocyte binding to the endothelium. The nuclear factor-κB (NF-κB) system appears to regulate the expression of many of the genes involved in this process. Angiotensin II contributes to atherogenesis by increasing expression of many pro-inflammatory genes, in part by inducing oxidative stress, which activates NF-κB.
No takes yet. Share an insight, caveat, or question.
Caterina et al. (2003) conducted a review in Atherosclerotic vascular disease. ACE inhibition was evaluated. Angiotensin II contributes to atherogenesis by increasing expression of pro-inflammatory genes and inducing oxidative stress, which activates the NF-κB system.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: