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Curr Heart Fail Rep. 2012 Jun;9(2):92-100. doi: 10.1007/s11897-012-0088-6.

TNF revisited: osteoprotegerin and TNF-related molecules in heart failure.

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1
Research Institute of Internal Medicine, Faculty of Medicine, Rikshospitalet, Oslo University Hospital, Sognsvannsveien 20, 0027, Oslo, Norway. thor.ueland@medisin.uio.no

Abstract

The pathophysiological role of tumor necrosis factor (TNF) in myocardial failure has been extensively examined in experimental and clinical studies. Recent studies suggest that other members of the TNF/TNF receptor superfamily (TNFSF/TNFRSF) also may play a pathogenic role in chronic HF. TNF ligands, and in particular members of the TNFRSF, are expressed by a wide variety of cells, including myocardial cells. By activating the nuclear factor-κB (NF-κB) and death-related pathways, TNF ligands can induce a variety of effects within the myocardium, including apoptosis, hypertrophy, inflammation, and extracellular matrix remodeling. Among several TNFSF members that have been shown activated in HF, the OPG/RANK/RANKL (osteoprotegerin/receptor activator of NF-κB/RANK ligand) axis may be of importance in the pathogenesis of this disorder through different mechanisms. In this paper, we revisited the role of TNFSF/TNFRSF in the pathophysiology of HF, possibly representing new targets for therapy as well as new biomarkers in this disorder.

PMID:
22453763
DOI:
10.1007/s11897-012-0088-6
[Indexed for MEDLINE]
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