Heart tumor necrosis factor

O, Corti A, Cassani G, Visioli O Tumor necrosis factor-soluble receptors in patients with various degrees of congestive heart failure. Circulation 1995 92 1479. si... 

RD, Young JB, Mann DL Tumor necrosis factor-a and tumor necrosis factor receptors in the failing human heart. Circulation 1996 93 704. 52... 

Inflammatory cytokines have been implicated in the pathophysiology of HF.9 Several proinflammatory (e.g., tumor necrosis factor-a [TNF-a], interleukin-1, interleukin-6, and interferon-y) and anti-inflammatory cytokines (e.g., interleukin-10) are overexpressed in the failing heart. The most is known about TNF-a, a pleiotrophic cytokine that acts as a negative inotrope, stimulates cardiac cell apoptosis, uncouples 3-adrenergic receptors from adenylyl cyclase, and is related to cardiac cachexia. The exact role of cytokines and inflammation in HF pathophysiology continues to be studied. 

Y., Kawamura, N. Feldman, A. M., Tsutsui, H., Shimokawa, H., Takeshita, A., Involvement of inducible nitric oxide synthase in cardiac dysfunction with tumor necrosis factor-alpha, Am. J. Physiol. Heart Circ. Physiol. 282 (2002),... 

Kwon HJ, Cote TR, Cuffe MS, Kramer JM, Braun MM. Case reports of heart failure after therapy with a tumor necrosis factor antagonist. Ann Intern Med 2003 138 807-11. 

Etanercept is a recombinant human soluble tumor necrosis factor-alpha (TNFo ) receptor fusion protein that binds to TNFo and decreases its role in disorders involving excess inflammation. It is approved for subcutaneous use in the treatment of patients with moderate to severe active rheumatoid arthritis, juvenile rheumatoid arthritis, psoriatic arthritis, ankylosing arthritis and plaque psoriasis. To the adverse reactions mentioned for infliximab, rare reports of congestive heart failure should be added. 

Skoog T, Dichtl W, Boquist S et al. Plasma tumor necrosis factor-a and early carotid atherosclerosis in healthy middle-aged men. Eur Heart J. 2002, 23 376-383. 

Herrmann S-M, Ricard S, Nicaud V et al. Polymorphisms of the tumor necrosis factor-a gene, coronary heart disease and obesity. Eur J Clin Invest. 1998, 28 59-66. 

Vendrell J, Fernandez-Real J-M, Gutierrez C, Zamora A, Simon I, Bardaji A, Ricart W, Richart C. A polymorphism in the promoter of the tumor necrosis factor-a gene (-308) is associated with coronary heart disease in type 2 diabetic patients. Atherosclerosis. 2003, 167 257-264. 

Oral, H., Kapadia, S., Nakano, M. et al. (1995). Tumor necrosis factor alpha and the failing heart. Clin. Cardiol. 18, IV20-IV27... 

Since oxidative stress has been reported to produce subcellular redistribution and activation of NF-kB, we measured total NF-kB content in cytosolic and particulate fractions of the hearts subjected to ischemia/reperfusion. In another set of experiments, the activation of NF-kB protein was studied by measuring the total NF-kB and phospho-NF-KB in the heart homogenate. Elevated ratios of NF-kB in particulate versus cytosolic fraction and of phospho-NF-KB and total NF-kB in the hearts subjected to ischemia/reperfusion were reduced by selenium. As oxidative stress has been reported to produce subcellular redistribution and activation of NF-kB and antioxidants have been shown to prevent this alteration (Cargnoni et al. 2002), it is possible that our observation on selenium-induced NF-kB translocation might be due to its antioxidant action. It should be noted that since selenium treatment could reduce the tumor necrosis factor-cc (TNF-ct)-mediated activation of NF-kB (Kim and Stadtman 1997), it suggests a possible involvement of a reduction in the formation of TNF-tx in the hearts subjected to ischemia/reperfusion by selenium. 

Tumor Necrosis Factor Alpha Tumor necrosis factor alpha (TNFa) is an inflammatory cytokine and interleukin that is involved in the genesis of sepsis, arthritis, and a variety of other inflammatory states (see Chapter 22). It also has hemodynamic effects and reduces ventricular performance. It is also a common signaling molecule. Assays for it or its receptor have been developed, but the failure of recent therapeutic trials has led to concern about how to properly interpret the high levels seen in patients with CHF and coronary heart disease. At present, there are no standardized assays and no reference interval studies or consistent assay validations. 

T. Yokoyama, L. Vaca, W. Durante, P. Hazarika and D. L. Mann, Cellular basis for the negative inotropic effects of tumor necrosis factor-a in the adult mammalian heart, J Clin Invest 92,2303-2312 (1993). 

D. R. Meldrum, Tumor necrosis factor in the heart, Am J Physiol Regul Integ Comp Physiol 274, R577-R595 (1998). 

Chung ES, Packer M, Lo KH, et al. Randomized, double-bUnd, placebo-controlled, pilot trial of infliximab, a chimeric monoclonal antibody to tumor necrosis factor-alpha, in patients with moderate-to-severe heart failure Results of the anti-TNF Therapy Against Congestive Heart Failure (ATTACH) trial. Circulation 2003 107 3133-3140. 

Many of the manifestations of intraabdominal infections, particularly peritonitis, result from cytokine activity. Inflammatory cytokines, such as tumor necrosis factor a (TNF-a), interleukin 1 (IL-1), IL-6, IL-8, and interferon-y (INF-y), are produced by macrophages and neutrophils in response to bacteria and bacterial products or in response to tissue injury resulting from the surgical incision. These cytokines produce wide-ranging effects on the endothelium of organs, particularly the liver, lungs, kidneys, and heart. With uncontrolled activation of these mediators, sepsis may result (see Chap. 117). 

C24. Chollet Martin, S., Depoix, J. P., Hvass, U., Pansard, Y., Vissuzaine, C., and Gougerot Pocidalo, M. A. Raised plasma levels of tumor necrosis factor in heart allograft rejection. Transplant. Proc. 22, 283-286 (1990). 

Vadlamani L, Lyenger S (2004). Tumor necrosis factor alpha polymorphism in heart failure/cardiomyopathy. Congest. Heart Failure. 10 289-292. 

Clausell, N., de Lima, V.C., Molossi, S., Liu, P., Turley, E., Gotlieb, A.I., Adelman, A.G., and Rabinovitch, M. (1995) Expression of Tumor Necrosis Factor Alpha and Accumulation of Fibronectin in Coronary Artery Restenotic Lesions Retrieved by Atherectomy, Br. Heart. J. 73,534-539. 

Levine, B., Kalman, J., Mayer, L., FUht, H.M., Packer, M. (1990). Elevated circulating levels of tumor necrosis factor in severe chronic heart failure. N. Engl. J. Med. 323(4) 236-241. 

Nishio R, Matsumori A, Shioi T, Wang W, Yamada T, Ono K, Sasayama S. Denopamine, a beta 1-adrenergic agonist, prolongs survival in a murine model of congestive heart failure induced by viral myocarditis suppression of tumor necrosis factor-alpha production in the heart. J. Am. Coll. Cardiol. 1998 32(3) 808-815. 

Vaddi K, Nicolini FA, Mehta P, Mehta JL. Increased secretion of tumor necrosis factor-alpha and interferon-gamma by mononuclear leukocytes in patients with ischemic heart disease. Circulation 1994 90 694-699. 

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