Potential Role of Nuclear Factor κB in Cardiovascular Disease

Abstract

Lung and Cardiovascular disease creating a major health burden in developed countries and primary cause of deaths. Although treatments have progressed, the development of novel treatments for patients with cardiovascular diseases remains a major research goal. Despite modern advances in pharmacological and interventional cardiology, cardiovascular disease still remains a leading cause of morbidity and mortality in all over the world. The nuclear factor (NF)-?B super family of transcription factors has been implicated in the regulation of immune cell maturation, cell survival, and inflammation in many cell types, including cardiac myocytes. Recent studies have shown that NF-?B is cardioprotective during acute hypoxia and reperfusion injury. NF-kB regulates the gene expression of major pro-inflammatory cytokines (TNF-a, IL-b), chemokines [macrophage inflammatory protein (MIP-2), cytokine-induced neutrophil chemoattractant (CINC)], and adhesion molecules (ICAM-1, E selectin) (2), all of which play a major role in lung injury. However, prolonged activation of NF-?B appears to be detrimental and promotes heart failure by eliciting signals that trigger chronic inflammation through enhanced elaboration of cytokines. In this review, we summarize progresses in understanding the NF-kB pathway in lung and cardio-vascular disease development as well as in modulating NF-kB for prevention and therapy.