15 research outputs found
Onc-gene expression in hyperplasia induced by tape stripping or by topical application of TPA
Tumor Necrosis Factor alpha converting enzyme (TACE), a newly identified target of MMP-3
Effect of NAC given as a therapeutic treatment against hypertension-induced cardiac remodeling
Low-molecular weight and unfractionated heparins induce a downregulation of inflammation: decreased levels of proinflammatory cytokines and nuclear factor-kappaB in LPS-stimulated human monocytes
Cardiac glutathione content determines cardiac function alterations in hypertensive L-NAME rat
Cardiac glutathione content determines cardiac function alterations in hypertensive L-NAME rat
Tumor necrosis factor alpha and glutathione interplay in chronic heart failure.
The pro-inflammatory cytokine, tumor necrosis factor alpha (TNF alpha), in concert with neurohormones, contributes to chronic heart failure (CHF) progression. This implies that TNF alpha antagonism may constitute an important target for CHF therapy. However, clinical trials in CHF patients using compounds that trap TNF alpha comprising infliximab, an antibody directed to TNF alpha, and etanercept, a soluble recombinant receptor of TNF alpha, gave disappointing results bringing back to light the dual, short-term beneficial and long-term harmful effect of TNF a.
This review focuses on the dual, concentration- and time-related effects of TNF alpha, the yin and yang action of TNF alpha in cardiac ischemia/reperfusion and contraction. Importantly, the harmful, effects of TNF alpha. are related to glutathione deficiency, a common hallmark to several other chronic inflammatory diseases. Recently, in rat models of CHF, oral administration of the glutathione precursor, N-acetylcysteine (NAC), was shown to hinder pathways of TNF alpha harmful signalling and to rescue cardiac structure and function