The role of interleukin-1 in the failing heart

被引：25

作者：

Maan D.L. ^{[1
]}

机构：

[1] Cardiology Section, Denver Health Medical Center, University of Colorado, Denver

来源：

Heart Failure Reviews | 2001年 / 6卷 / 2期

基金：

美国国家卫生研究院;

关键词：

Cytokine; Gene expression; Heart failure; Interleukin-1; Myocyte;

D O I：

10.1023/A:1011428824771

中图分类号：

学科分类号：

摘要：

The prevalence of congestive heart failure and its continued poor prognosis despite presently available therapeutic options emphasize the importance of pursuing the observations suggesting an important role for an immunomodulatory approach to decompensated cardiac failure. Furthermore, there are several pieces of background information that suggest that cytokines like IL-1 may play a significant role in the pathogenesis of several forms of myocardial dysfunction. Although it seems clear that IL-1 is not acting alone under circumstances of myocardial injury, but in concert with other pro-inflammatory molecules and their effectors, we believe that continued investigations into the cytokine hypothesis will ultimately increase the understanding of how pro-inflammatory molecules influence myocardial function and how the modulation of such factors may improve the myocardial response to injury. The specific observations that emphasize the importance of pursuing a substantive role for IL-1 in this process are: (1) IL-1 is elevated in several cardiac disease states, (2) IL-1 is produced by myocardial cells themselves in response to injury, (3) The alterations in gene expression seen in response IL-1 resembles in many ways the phenotype of the failing heart, and (4) The co-localization of the IL-1 response with that of several previously described negative transcriptional regulators (making them potential targets for therapeutic manipulation).

引用

页码：81 / 94

页数：13

共 96 条

[1]

Mauviel A., Cytokine regulation of metalloproteinase gene expression, J Cell Biochem, 53, pp. 288-295, (1993)

[2]

Booz G.W., Baker K.M., Molecular signalling mechanisms controlling growth and function of cardiac fibroblasts, Cardiovasc Res, 30, pp. 537-543, (1995)

[3]

Li Y.Y., McTiernan C.F., Feldman A.M., Proinflammatory cytokines regulate tissue inhibitors of metalloproteinases and disintegrin metalloproteinase in cardiac cells, Cardiovasc Res, 42, pp. 162-172, (1999)

[4]

Palmer J.N., Hartogensis W.E., Patten M., Fortuin F.D., Long C.S., Interleukin-1 beta induces cardiac myocyte growth but inhibits cardiac fibroblast proliferation in culture, J Clin Invest, 95, pp. 2555-2564, (1995)

[5]

Patten M., Hartogensis W.E., Long C.S., IL-1β is a negative regulator of α<sub>1</sub>-adrenergic induced cardiac gene expression, J Biol Chem, 271, pp. 21134-21141, (1996)

[6]

Thaik C.M., Calderone A., Takahashi N., Colucci W.S., Interleukin-1 beta modulates the growth and phenotype of neonatal rat cardiac myocytes, J Clin Invest, 96, pp. 1093-1099, (1995)

[7]

McTiernan C.F., Lemster B.H., Frye C., Brooks S., Combes A., Feldman A.M., Interleukin-1 beta inhibits phospholamban gene expression in cultured cardiomyocytes, Circ Res, 81, pp. 493-503, (1997)

[8]

Kacimi R., Long C.S., Karliner J.S., Chronic hypoxia modulates the interleukin-1beta-stimulated inducible nitric oxide synthase pathway in cardiac myocytes, Circulation, 96, pp. 1937-1943, (1997)

[9]

Kacimi R., Karliner J.S., Koudssi F., Long C.S., Expression and regulation of adhesion molecules in cardiac cells by cytokines, Circ Res, 82, pp. 576-586, (1998)

[10]

LaPointe M.C., Isenovic E., Interleukin-1beta regulation of inducible nitric oxide synthase and cyclooxygenase-2 involves the p42/44 and p38 MAPK signaling pathways in cardiac myocytes, Hypertension, 33, pp. 276-282, (1999)

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