Nuclear factor kappa-B and the heart

Nuclear factor kappa-B (NF kappaB), a redox-sensitive transcription factor regulating a battery of inflammatory genes, has been indicated to play a role in the development of numerous pathological states. Activation of NF kappaB induces gene programs leading to transcription of factors that promote inflammation, such as leukocyte adhesion molecules, cytokines, and chemokines, although some few substances with possible anti-inflammatory effects are also NF kappaB regulated. The present article reviews basic regulation of NF kappaB and its activation, cell biological effects of NF kappaB activation and the role of NF kappaB in apoptosis. Evidence involving NF kappaB as a key factor in the pathophysiology of ischemia-reperfusion injury and heart failure is discussed. Although activation of NF kappaB induces pro-inflammatory genes, it has lately been indicated that the transcription factor is involved in the signaling of endogenous myocardial protection evoked by ischemic preconditioning. A possible role of NF kappaB in the development of atherosclerosis and unstable coronary syndromes is discussed. Nuclear factor kappa-B may be a new therapeutic target for myocardial protection. (Am Loll Cardiol 2001;38:307-14) (C) 2001 by the American College of Cardiology.