Sökning: onr:"swepub:oai:prod.swepub.kib.ki.se:119675999" >
Doxorubicin acts th...
Doxorubicin acts through tumor necrosis factor receptor subtype 1 to cause dysfunction of murine skeletal muscle
-
Gilliam, LAA (författare)
-
Ferreira, LF (författare)
-
- Bruton, JD (författare)
- Karolinska Institutet
-
visa fler...
-
Moylan, JS (författare)
-
- Westerblad, H (författare)
- Karolinska Institutet
-
Clair, DKS (författare)
-
Reid, MB (författare)
-
visa färre...
-
(creator_code:org_t)
- American Physiological Society, 2009
- 2009
- Engelska.
-
Ingår i: Journal of applied physiology (Bethesda, Md. : 1985). - : American Physiological Society. - 1522-1601 .- 8750-7587. ; 107:6, s. 1935-1942
- Relaterad länk:
-
https://europepmc.or...
-
visa fler...
-
http://kipublication...
-
https://doi.org/10.1...
-
visa färre...
Abstract
Ämnesord
Stäng
- 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.
Publikations- och innehållstyp
- ref (ämneskategori)
- art (ämneskategori)
Hitta via bibliotek
Till lärosätets databas