Abstract
Cardiovascular diseases and diabetes are the leading cause of morbidity and mortality in all countries. Atherosclerosis, the background for many cardiovascular diseases, is characterized by the accumulation of lipid and fibrotic entities in large arteries and bears many similarities with chronic inflammatory diseases such as diabetes. Common features include extravasation of blood-derived leukocytes, as well as production of cytokines, chemokines and matrix-degrading enzymes. There are also many shared signaling pathways, including activation of the nuclear factor kB (NF-kB) cascade. In the pathology of atherosclerosis and diabetes NF-kB is essential to the cross-talk between cytokines, adhesion molecules and growth factors, leading to atherosclerotic plaque formation, growth and eventual rupture. The intent of this paper is to gather and summarize information on the role of NF-kB in the pathology of atherosclerosis and diabetes. Thus, it is essential to understand the role of this important signaling cascade in atherosclerosis and diabetes, in a quest for more specific therapeutic targets.
Highlights
Introduction ofSN50 into cell efficiently inhibits LPS — and TNFα-induced nuclear factor kB (NF-kB) nuclear translocation and reduces NF-kB DNA binding in cultured endothelial and monocytic cells [56].26S proteasome inhibitors prevent IkBα degradation and NF-kB activation
An inhibitory effect on NF-kB has been proposed for 4 -hydroxynonenal, one of the most abundant aldehydes formed during oxidation of LDL, which has been reported to inhibit NF-kB-dependent transcriptional activation of inducible nitric oxide (NO) synthase in smooth muscle cells [34]
In contrast to human cells, deletion of IkB kinase (IKK)-2 in murine macrophages was associated with reduced tumor necrosis factor a (TNFa), IL-6 and IL-10 production, in the absence of any modification of LPS-induced modified LDL uptake [25]
Summary
Introduction ofSN50 into cell efficiently inhibits LPS — and TNFα-induced NF-kB nuclear translocation and reduces NF-kB DNA binding in cultured endothelial and monocytic cells [56].26S proteasome inhibitors prevent IkBα degradation and NF-kB activation. An inhibitory effect on NF-kB has been proposed for 4 -hydroxynonenal, one of the most abundant aldehydes formed during oxidation of LDL, which has been reported to inhibit NF-kB-dependent transcriptional activation of inducible nitric oxide (NO) synthase (iNOS) in smooth muscle cells [34].
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