ArticleAmerican journal of physiology. Lung cellular and molecular physiology2011
TNF/TNFR1 signaling mediates doxorubicin-induced diaphragm weakness.
Article in American journal of physiology. Lung cellular and molecular physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.
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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.
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Who cites it
25 citing papers in PubMed, 1 synthesis or guideline pooled it, 42 citations in OpenAlex.
- Doxorubicin-induced skeletal muscle atrophy: Elucidating the underlying molecular pathways.Acta physiologica (Oxford, England) · 2020Pooled it
- Ameliorative effects of agomelatine against doxorubicin-induced hepatotoxicity.BMC pharmacology & toxicology · 2025Article
- Pera orange juice (Heliyon · 2024Article
- Effects of exercise and doxorubicin on acute diaphragm neuromuscular transmission failure.Experimental neurology · 2024Article
- Liraglutide Pretreatment Does Not Improve Acute Doxorubicin-Induced Cardiotoxicity in Rats.International journal of molecular sciences · 2024Article
- Article
- Skeletal muscle fibers play a functional role in host defense during sepsis in mice.Scientific reports · 2021Article
- Review
- The Etiology and Impact of Muscle Wasting in Metastatic Cancer.Cold Spring Harbor perspectives in medicine · 2020Review
- The role of inflammation in adjuvant chemotherapy-induced sarcopenia (Izmir Oncology Group (IZOG) study).Supportive care in cancer : official journal of the Multinational Association of Supportive Care in Cancer · 2020Observational
- The Impact of Immune Cells on the Skeletal Muscle Microenvironment During Cancer Cachexia.Frontiers in physiology · 2020Review
- Exercise stimulates beneficial adaptations to diminish doxorubicin-induced cellular toxicity.American journal of physiology. Regulatory, integrative and comparative physiology · 2019Review
- Chronic doxorubicin administration impacts satellite cell and capillary abundance in a muscle-specific manner.Physiological reports · 2019Article
- The regulation of skeletal muscle fatigability and mitochondrial function by chronically elevated interleukin-6.Experimental physiology · 2019Article
- Treadmill Exercise Ameliorates Chemotherapy-Induced Muscle Weakness and Central Fatigue by Enhancing Mitochondrial Function and Inhibiting Apoptosis.International neurourology journal · 2019Article
- Docetaxel does not impair skeletal muscle force production in a murine model of cancer chemotherapy.Physiological reports · 2017Article
- Doxorubicin inhibits muscle inflammation after eccentric exercise.Journal of cachexia, sarcopenia and muscle · 2017Article
- Article
- Systemic blockade of ACVR2B ligands prevents chemotherapy-induced muscle wasting by restoring muscle protein synthesis without affecting oxidative capacity or atrogenes.Scientific reports · 2016Article
- Targeted overexpression of mitochondrial catalase protects against cancer chemotherapy-induced skeletal muscle dysfunction.American journal of physiology. Endocrinology and metabolism · 2016Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Doxorubicin, a common chemotherapeutic agent, causes respiratory muscle weakness in both patients and rodents. Tumor necrosis factor-α (TNF), a proinflammatory cytokine that depresses diaphragm force, is elevated following doxorubicin chemotherapy. TNF-induced diaphragm weakness is mediated through TNF type 1 receptor (TNFR1). These findings lead us to hypothesize that TNF/TNFR1 signaling mediates doxorubicin-induced diaphragm muscle weakness. We tested this hypothesis by treating C57BL/6 mice with a clinical dose of doxorubicin (20 mg/kg) via intravenous injection. Three days later, we measured contractile properties of muscle fiber bundles isolated from the diaphragm. We tested the involvement of TNF/TNFR1 signaling using pharmaceutical and genetic interventions. Etanercept, a soluble TNF receptor, and TNFR1 deficiency protected against the depression in diaphragm-specific force caused by doxorubicin. Doxorubicin stimulated an increase in TNFR1 mRNA and protein (P < 0.05) in the diaphragm, along with colocalization of TNFR1 to the plasma membrane. These results suggest that doxorubicin increases diaphragm sensitivity to TNF by upregulating TNFR1, thereby causing respiratory muscle weakness.
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Registered trials
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