Inflammation meets oxidation: NF-kappaB as a mediator of initial lesion development in atherosclerosis.
Transcription factor nuclear factor-kappaB (NF-kappaB) and its target genes are involved in the pathogenesis of atherosclerosis, in addition to many other diseases. Monocyte recruitment into subendothelial space is primarily mediated by NF-kappaB-dependent gene expression, and this event is a crucial milestone, because it is nearly impossible to reverse the progression of the lesion after this point. Recent advances in our understanding of atherosclerosis as a disease of childhood enforces the necessity of developing novel approaches for prevention and treatment. Here, the authors address NF-kappaB as a major therapeutic target, especially for preventive measures, in the light of two main hypotheses of atherosclerosis: oxidation and inflammation.
Kutuk
Ozgur
O
Biological Sciences and Bioengineering Program, Sabanci University, 34956 Orhanli-Tuzla, Istanbul, Turkey.
Basaga
Huveyda
H
D000818:Animals; D001161:Arteriosclerosis / Q000378:metabolism* / Q000473:pathology; D002448:Cell Adhesion; D006801:Humans; D007249:Inflammation; D008954:Models, Biological; D016328:NF-kappa B / Q000378:metabolism / Q000502:physiology*; D010100:Oxygen / Q000378:metabolism*
D016328:NF-kappa B; D010100:Oxygen