Nuclear factor kappa-B (NFkappaB), 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 NFkappaB 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 NFkappaB regulated. The present article reviews basic regulation
of NFkappaB and its activation, cell biological effects of NFkappaB activation and
the role of NFkappaB in apoptosis. Evidence involving NFkappaB as a key factor in
the pathophysiology of ischemia-reperfusion injury and heart failure is discussed.
Although activation of NFkappaB 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 NFkappaB
in the development of atherosclerosis and unstable coronary syndromes is discussed.
Nuclear factor kappa-B may be a new therapeutic target for myocardial protection.