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