Key result
The ambivalent nature of NF-kappaB, which mediates both deleterious hypertrophic signals and protective nitric oxide production, may limit the therapeutic use of NF-kappaB inhibitors.
The ambivalent role of NF-kappaB in both promoting hypertrophy and stimulating protective nitric oxide production complicates the potential therapeutic use of NF-kappaB inhibitors in heart remodelling.
NF-κB inhibition warrants caution in remodeling; leaves open selective targeting for future studies.
Hypertrophy of the myocardium is induced by haemodynamic and humoral alterations, which in turn stimulate the production of factors triggering protein synthesis, thus initiating myocardial growth. It has recently been documented that nuclear factor kappa B (NF-kappaB) represents a key factor that mediates both neurohormonal and proinflammatory signals leading finally to hypertrophic and/or fibrotic processes in the cardiovascular system. It was suggested that blockade of NF-kappaB may exert a protective effect against pathological myocardial growth. Recent data indicate that increased activity of NF-kappaB, besides its deleterious effects, leads to the increased production of nitric oxide, which as a result of its hypotensive and antigrowth activity exerts protection against the hypertrophic and proliferative processes. This ambivalent nature of NF-kappaB might limit the use of NF-kappaB inhibitors for therapeutic purposes and should evoke further studies to clarify unequivocally the nature of NF-kappaB inhibition in the haemodynamically overloaded circulation.
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Pecháňová et al. (2010) conducted a review in Myocardial hypertrophy and heart remodelling. NF-kappaB inhibitors was evaluated. The ambivalent nature of NF-kappaB, which mediates both deleterious hypertrophic signals and protective nitric oxide production, may limit the therapeutic use of NF-kappaB inhibitors.
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