Key result
Doxorubicin directly impaired ex vivo skeletal muscle relaxation and contraction in a time- and concentration-dependent manner, associated with increased calcium responses not explained by oxidative stress.
Why the study?
Does doxorubicin directly impair skeletal muscle function and calcium responses in preclinical models?
Does doxorubicin directly impair skeletal muscle function and calcium responses in preclinical models?
Doxorubicin directly impairs skeletal muscle relaxation and contraction via altered calcium responses independent of oxidative stress, contributing to chemotherapy-induced fatigue.
Answers are grounded in this paper and cite their sources.
Hypothesis-generating in animal models; leaves open whether calcium dysregulation drives doxorubicin-related fatigue in patients.
Chemotherapy-induced fatigue is a multidimensional symptom. Oxidative stress has been proposed as a working mechanism for anthracycline-induced cardiotoxicity. In this study, doxorubicin (DOX) was tested on skeletal muscle function. Doxorubicin induced impaired ex vivo skeletal muscle relaxation followed in time by contraction impediment, which could be explained by DOX-induced changes in Ca(2+) responses of myotubes in vitro. The Ca(2+) responses in skeletal muscle, however, could not be explained by oxidative stress.
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Norren et al. (2009) studied Chemotherapy-induced fatigue. Doxorubicin vs. Control (no doxorubicin) was evaluated on Skeletal muscle contractile characteristics (maximal force, relaxation velocity) and calcium influx (p=<0.05). Doxorubicin directly impaired ex vivo skeletal muscle relaxation and contraction in a time- and concentration-dependent manner, associated with increased calcium responses not explained by oxidative stress.
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