ArticleJournal of applied physiology (Bethesda, Md. : 1985)2009
Doxorubicin acts through tumor necrosis factor receptor subtype 1 to cause dysfunction of murine skeletal muscle.
Article in Journal of applied physiology (Bethesda, Md. : 1985), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
63 citing papers in PubMed, 1 synthesis or guideline pooled it, 103 citations in OpenAlex.
- Doxorubicin-induced skeletal muscle atrophy: Elucidating the underlying molecular pathways.Acta physiologica (Oxford, England) · 2020Pooled it
- No evidence for changes in skeletal muscle mass or weight during first-line chemotherapy for metastatic colorectal cancer.BMC cancer · 2019Trial
- Trial
- Chemotherapy-Induced Skeletal Muscle Dysfunction and Cognitive Impairment: A Muscle-Brain Mechanistic Framework With Implications for Exercise Oncology.Journal of cachexia, sarcopenia and muscle · 2026Review
- Mechanisms, assessment, and exercise interventions for skeletal muscle dysfunction post-chemotherapy in breast cancer: from inflammation factors to clinical practice.Frontiers in oncology · 2025Review
- Restoring Skeletal Muscle Health through Exercise in Breast Cancer Patients and after Receiving Chemotherapy.International journal of molecular sciences · 2024Review
- Evaluation of skeletal muscle function in male rats with doxorubicin-induced myopathy following various exercise techniques: the significant role of glucose transporter 4.Pflugers Archiv : European journal of physiology · 2024Article
- Article
- An electrical stimulation intervention protocol to prevent disuse atrophy and muscle strength decline: an experimental study in rat.Journal of neuroengineering and rehabilitation · 2023Article
- Tumor-associated macrophages induce inflammation and drug resistance in a mechanically tunable engineered model of osteosarcoma.Biomaterials · 2023Article
- Chemotherapy-Induced Molecular Changes in Skeletal Muscle.Biomedicines · 2023Review
- Proteasomal Degradation of TRAF2 Mediates Mitochondrial Dysfunction in Doxorubicin-Cardiomyopathy.Circulation · 2022Article
- Calotropis gigantea stem bark extracts inhibit liver cancer induced by diethylnitrosamine.Scientific reports · 2022Article
- Chemotherapy agents reduce protein synthesis and ribosomal capacity in myotubes independent of oxidative stress.American journal of physiology. Cell physiology · 2021Article
- Comparative Study of the Pharmacological Properties and Biological Effects ofPharmaceutics · 2021Article
- Review
- Tumor Necrosis Factor Alpha-Mediated Inflammation and Remodeling of the Extracellular Matrix Underlies Aortic Stiffening Induced by the Common Chemotherapeutic Agent Doxorubicin.Hypertension (Dallas, Tex. : 1979) · 2021Article
- Review
- The Etiology and Impact of Muscle Wasting in Metastatic Cancer.Cold Spring Harbor perspectives in medicine · 2020Review
- Doxorubicin-Induced Oxidative Stress and Endothelial Dysfunction in Conduit Arteries Is Prevented by Mitochondrial-Specific Antioxidant Treatment.JACC. CardioOncology · 2020Article
3 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 3 countries.
Funding
Abstract
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-alpha (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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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.