The DOI matches its Crossref record; 77 of the 77 references it cites were found in a registry or an index.
Inflammatory Mediators and the Failing Heart: Past, Present, and the Foreseeable Future
Abstract
Recent studies have identified the importance of proinflammatory mediators in the development and progression of heart failure. The growing appreciation of the pathophysiological consequences of sustained expression of proinflammatory mediators in preclinical and clinical heart failure models culminated in a series of multicenter clinical trials that used “targeted” approaches to neutralize tumor necrosis factor in patients with moderate to advanced heart failure. However, these targeted approaches have resulted in worsening heart failure, thereby raising a number of important questions about what role, if any, proinflammatory cytokines play in the pathogenesis of heart failure. This review will summarize the tremendous growth of knowledge that has taken place in this field, with a focus on what we have learned from the negative clinical trials, as well as the potential direction of future research in this area.
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Cites
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Plasma Norepinephrine as a Guide to Prognosis in Patients with Chronic Congestive Heart Failure
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Elevated Circulating Levels of Tumor Necrosis Factor in Severe Chronic Heart Failure
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“”9,14 Regarding the potential mechanisms for the deleterious effects of TNF on LV function, the literature suggests that TNF modulates myocardial function through at least two different pathways: (1) an immediate pathway that is manifest within minutes and is mediated by activation of the neutral sphingomyelinase path…”
BackgroundShock and Tissue Injury Induced by Recombinant Human Cachectin
Tracey, K. J., Beutler, B., Lowry, S. F., Merryweather, J., Wolpe, S., Milsark, I. W., Hariri, R. J., Fahey, T. J., Zentella, A., Albert, J. D., et al. (1986) · Science · doi:10.1126/science.3764421 · Cited by 2,549
Immunosuppressive effects of apoptotic cells
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Negative Inotropic Effects of Cytokines on the Heart Mediated by Nitric Oxide
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Treatment of Septic Shock with the Tumor Necrosis Factor Receptor:Fc Fusion Protein
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Self-citation
Cited by
Mitochondrial DNA that escapes from autophagy causes inflammation and heart failure
Oka, T., Hikoso, S., Yamaguchi, O., Taneike, M., Takeda, T., Tamai, T., Oyabu, J., Murakawa, T., Nakayama, H., Nishida, K., et al. (2012) · Nature · doi:10.1038/nature10992 · Cited by 1,201
Tham, Y. K., Bernardo, B. C., Ooi, J. Y. Y., Weeks, K. L., & McMullen, J. R. (2015) · Archives of Toxicology · doi:10.1007/s00204-015-1477-x · Cited by 708
Inflammatory mediators in chronic heart failure: an overview
Anker, S. D., & von Haehling, S. (2004) · Heart · doi:10.1136/hrt.2002.007005 · Cited by 627
Animal Models of Heart Failure: A Scientific Statement From the American Heart Association
Houser, S. R., Margulies, K. B., Murphy, A. M., Spinale, F. G., Francis, G. S., Prabhu, S. D., Rockman, H. A., Kass, D. A., Molkentin, J. D., Sussman, M. A., et al. (2012) · Circulation Research · doi:10.1161/res.0b013e3182582523 · Cited by 435
Eriksson, U., Ricci, R., Hunziker, L., Kurrer, M. O., Oudit, G. Y., Watts, T. H., Sonderegger, I., Bachmaier, K., Kopf, M., & Penninger, J. M. (2003) · Nature Medicine · doi:10.1038/nm960 · Cited by 405
Metadata
- Authors
- Mann, D. L.
- Venue
- Circulation Research
- Published
- 2002-11-29
- Volume
- 91
- Issue
- 11
- Pages
- 988-998
- ISSN
- 0009-7330 (ISSN-L)
- 1524-4571
- OpenAlex
- W2136094484
- Cited by
- 988
- References
- 77
- FWCI
- 24.91
- Type
- journal article
- Language
- en
- Open access
- closed
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- CoChat. (2026). Citation check: Inflammatory Mediators and the Failing Heart: Past, Present, and the Foreseeable Future. https://app.cochat.ai/papers/10.1161/01.res.0000043825.01705.1b
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- Mann, D. L. (2002). Inflammatory Mediators and the Failing Heart: Past, Present, and the Foreseeable Future. Circulation Research. https://doi.org/10.1161/01.res.0000043825.01705.1b
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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