Title : TNF/TNFR1 signaling mediates doxorubicin-induced diaphragm weakness.

Pub. Date : 2011 Feb

PMID : 21097524






6 Functional Relationships(s)
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1 TNF/TNFR1 signaling mediates doxorubicin-induced diaphragm weakness. Doxorubicin tumor necrosis factor Homo sapiens
2 Tumor necrosis factor-alpha (TNF), a proinflammatory cytokine that depresses diaphragm force, is elevated following doxorubicin chemotherapy. Doxorubicin tumor necrosis factor Homo sapiens
3 Tumor necrosis factor-alpha (TNF), a proinflammatory cytokine that depresses diaphragm force, is elevated following doxorubicin chemotherapy. Doxorubicin tumor necrosis factor Homo sapiens
4 These findings lead us to hypothesize that TNF/TNFR1 signaling mediates doxorubicin-induced diaphragm muscle weakness. Doxorubicin tumor necrosis factor Homo sapiens
5 Etanercept, a soluble TNF receptor, and TNFR1 deficiency protected against the depression in diaphragm-specific force caused by doxorubicin. Doxorubicin tumor necrosis factor Homo sapiens
6 These results suggest that doxorubicin increases diaphragm sensitivity to TNF by upregulating TNFR1, thereby causing respiratory muscle weakness. Doxorubicin tumor necrosis factor Homo sapiens