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Doxorubicin acts th...
Doxorubicin acts through tumor necrosis factor receptor subtype 1 to cause dysfunction of murine skeletal muscle
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Gilliam, LAA (author)
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Ferreira, LF (author)
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- Bruton, JD (author)
- Karolinska Institutet
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Moylan, JS (author)
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- Westerblad, H (author)
- Karolinska Institutet
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Clair, DKS (author)
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Reid, MB (author)
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(creator_code:org_t)
- American Physiological Society, 2009
- 2009
- English.
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In: Journal of applied physiology (Bethesda, Md. : 1985). - : American Physiological Society. - 1522-1601 .- 8750-7587. ; 107:6, s. 1935-1942
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Abstract
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- Cancer patients receiving doxorubicin chemotherapy experience both muscle weakness and fatigue. One postulated mediator of the muscle dysfunction is an increase in tumor necrosis factor-α (TNF), a proinflammatory cytokine that mediates limb muscle contractile dysfunction through the TNF receptor subtype 1 (TNFR1). Our main hypothesis was that systemic doxorubicin administration would cause muscle weakness and fatigue. Systemic doxorubicin administration (20 mg/kg) depressed maximal force of the extensor digitorum longus (EDL; P < 0.01), accelerated EDL fatigue ( P < 0.01), and elevated serum TNF levels ( P < 0.05) 72 h postinjection. Genetic TNFR1 deficiency prevented the fall in specific force caused by systemic doxorubicin, without protecting against fatigue ( P < 0.01). These results demonstrate that clinical doxorubicin concentrations disrupt limb muscle function in a TNFR1-dependent manner.
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- art (subject category)
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