ArticlePloS one2017
Cyclophosphamide leads to persistent deficits in physical performance and in vivo mitochondria function in a mouse model of chemotherapy late effects.
Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 38 citations in OpenAlex.
- Eating during immunotherapy sessions: a cross-sectional study of meal quality in patients with rheumatic diseases undergoing intravenous therapy with immunomodulators.Clinical rheumatology · 2026Article
- A review of soluble mediator and cytokine networks linking combination immunotherapy, tumor microenvironment remodeling and skeletal muscle dysfunction.Frontiers in immunology · 2026Review
- Comprehensive review of mouse models for studying cancer-related fatigue: Methods, findings and future directions (Review).Experimental and therapeutic medicine · 2025Review
- Dietary Carvacrol Attenuates Cyclophosphamide-Induced Neurotoxicity: Implications for Food-Derived Neuroprotection and Molecular Mechanisms.Food science & nutrition · 2025Article
- Associations between mitochondrial copy number, exercise capacity, physiologic cost of walking, and cardiac strain in young adult survivors of childhood cancer.Journal of cancer survivorship : research and practice · 2024Article
- A Comprehensive Review of Cancer Drug-Induced Cardiotoxicity in Blood Cancer Patients: Current Perspectives and Therapeutic Strategies.Current treatment options in oncology · 2024Review
- A single chemotherapy administration induces muscle atrophy, mitochondrial alterations and apoptosis in breast cancer patients.Journal of cachexia, sarcopenia and muscle · 2024Article
- Article
- Skeletal muscle mitochondrial interactome remodeling is linked to functional decline in aged female mice.Nature aging · 2023Article
- Elamipretide Improves ADP Sensitivity in Aged Mitochondria by Increasing Uptake through the Adenine Nucleotide Translocator (ANT).bioRxiv : the preprint server for biology · 2023Article
- Cachectic muscle wasting in acute myeloid leukaemia: a sleeping giant with dire clinical consequences.Journal of cachexia, sarcopenia and muscle · 2022Review
- Concurrence of osteonecrosis and steroid myopathy secondary to oral steroid therapy in a patient with ABCB1 gene polymorphisms: A case report.Frontiers in endocrinology · 2022Article
- A clinically relevant combination treatment with doxorubicin and cyclophosphamide does not induce hepatotoxicity in C57BL/6J mice.Liver research (Beijing, China) · 2021Article
- The Association of Mitochondrial Copy Number With Sarcopenia in Adult Survivors of Childhood Cancer.Journal of the National Cancer Institute · 2021Article
- Review
- Tumor regression and immunity in combination therapy with anti-CEA chimeric antigen receptor T cells and anti-CEA-IL2 immunocytokine.Oncoimmunology · 2021Article
- Skeletal Muscle Deconditioning in Breast Cancer Patients Undergoing Chemotherapy: Current Knowledge and Insights From Other Cancers.Frontiers in cell and developmental biology · 2021Review
- Alterations in Muscle Architecture: A Review of the Relevance to Individuals After Limb Salvage Surgery for Bone Sarcoma.Frontiers in pediatrics · 2020Article
- Impact of pharmacological agents on mitochondrial function: a growing opportunity?Biochemical Society transactions · 2019Review
- Immunohistochemical phenotyping of T cells, granulocytes, and phagocytes in the muscle of cancer patients: association with radiologically defined muscle mass and gene expression.Skeletal muscle · 2019Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Fatigue is the symptom most commonly reported by long-term cancer survivors and is increasingly recognized as related to skeletal muscle dysfunction. Traditional chemotherapeutic agents can cause acute toxicities including cardiac and skeletal myopathies. To investigate the mechanism by which chemotherapy may lead to persistent skeletal muscle dysfunction, mature adult mice were injected with a single cyclophosphamide dose and evaluated for 6 weeks. We found that exposed mice developed a persistent decrease in treadmill running time compared to baseline (25.7±10.6 vs. 49.0±16.8 min, P = 0.0012). Further, 6 weeks after drug exposure, in vivo parameters of mitochondrial function remained below baseline including maximum ATP production (482.1 ± 48.6 vs. 696.2 ± 76.6, P = 0.029) and phosphocreatine to ATP ratio (3.243 ± 0.1 vs. 3.878 ± 0.1, P = 0.004). Immunoblotting of homogenized muscles from treated animals demonstrated a transient increase in HNE adducts 1 week after exposure that resolved by 6 weeks. However, there was no evidence of an oxidative stress response as measured by quantitation of SOD1, SOD2, and catalase protein levels. Examination of mtDNA demonstrated that the mutation frequency remained comparable between control and treated groups. Interestingly, there was evidence of a transient increase in NF-ĸB p65 protein 1 day after drug exposure as compared to saline controls (0.091±0.017 vs. 0.053±0.022, P = 0.033). These data suggest that continued impairment in muscle and mitochondria function in cyclophosphamide-treated animals is not linked to persistent oxidative stress and that alternative mechanisms need to be considered.
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Registered trials
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