Associate Editor: G.F. BaxterTNFα in atherosclerosis, myocardial ischemia/reperfusion and heart failure
Section snippets
Tumor necrosis factor alpha: its formation, release and receptors
In 1975, tumor necrosis factor alpha (TNFα, cachexin or cachectin) was discovered as a circulating factor which can cause necrosis of tumors (Carswell et al., 1975).
More recently, TNFα has been identified as part of the innate immune system response to different forms of stresses [infection, trauma, ischemia/reperfusion (I/R)]. The innate immune system response is initiated independently from a specific antigen, and it uses pattern recognition receptors which when stimulated activate nuclear
Vascular effects of tumor necrosis factor alpha
The TNFα-mediated vascular dysfunction involves alterations in endothelial metabolism and function, platelet aggregation and EC–blood cell interaction, and in vascular smooth muscle cell (VSMC) function and proliferation (McKellar et al., 2009).
Tumor necrosis factor alpha and myocardial function
In healthy individuals, both the circulating and the cardiac TNFα concentrations are low (Aker et al., 2003, Arras et al., 1996, Frangogiannis et al., 1998). Supporting the notion that TNFα is of little physiological importance in the heart, TNFα-, TNFR1- and TNFR2 KO mice develop normally and have no discernable morphological or functional cardiac defects (Kurrelmeyer et al., 2000, Marino et al., 1997). Higher TNFα concentrations, however, alter myocardial function. Exogenous TNFα results in a
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