期刊
KIDNEY INTERNATIONAL
卷 87, 期 2, 页码 281-296出版社
ELSEVIER SCIENCE INC
DOI: 10.1038/ki.2014.285
关键词
tumor necrosis factor; tumor necrosis factor receptor-1; tumor necrosis factor receptor-2; renal dysfunction; inflammation; immunomodulatory; therapeutic
资金
- National Institute for Health Research Cambridge Biomedical Research Centre
- National Institutes of Health, NIDDK and NHLBI
Tumor necrosis factor (TNF), initially reported to induce tumor cell apoptosis and cachexia, is now considered a central mediator of a broad range of biological activities from cell proliferation, cell death and differentiation to induction of inflammation and immune modulation. TNF exerts its biological responses via interaction with two cell surface receptors: TNFR1 and TNFR2. (TNFRs). These receptors trigger shared and distinct signaling pathways upon TNF binding, which in turn result in cellular outputs that may promote tissue injury on one hand but may also induce protective, beneficial responses. Yet the role of TNF and its receptors specifically in renal disease is still not well understood. This review describes the expression of the INFRs, the signaling pathways induced by them and the biological responses of TNF and its receptors in various animal models of renal diseases, and discusses the current outcomes from use of TNF biologics and TNF biomarkers in renal disorders.
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