ArticleAmerican journal of physiology. Endocrinology and metabolism2016
Targeted overexpression of mitochondrial catalase protects against cancer chemotherapy-induced skeletal muscle dysfunction.
Article in American journal of physiology. Endocrinology and metabolism, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.
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Who cites it
35 citing papers in PubMed, 1 synthesis or guideline pooled it, 58 citations in OpenAlex.
- Doxorubicin-induced skeletal muscle atrophy: Elucidating the underlying molecular pathways.Acta physiologica (Oxford, England) · 2020Pooled it
- Effects of mitochondrial ABCB7 transporter upregulation on acute doxorubicin cardiorespiratory muscle injury.Journal of applied physiology (Bethesda, Md. : 1985) · 2026Article
- Mitochondrial-targeted plastoquinone therapy prevents early onset muscle weakness that occurs before atrophy during ovarian cancer.Molecular metabolism · 2025Article
- Cancer Cachexia.Advances in experimental medicine and biology · 2025Review
- Effect of preoperative physical activity on postoperative outcomes in esophageal cancer.Journal of physical therapy science · 2024Article
- Mitochondrial targeted catalase improves muscle strength following arteriovenous fistula creation in mice with chronic kidney disease.Scientific reports · 2024Article
- A single chemotherapy administration induces muscle atrophy, mitochondrial alterations and apoptosis in breast cancer patients.Journal of cachexia, sarcopenia and muscle · 2024Article
- Endurance exercise training reinforces muscular strength with improvements in mitochondrial oxidative capacity, lysosome reformation, and myogenic differentiation against doxorubicin-induced skeletal muscle wasting in mice.Physical activity and nutrition · 2023Article
- Inhibition of autophagy; an opportunity for the treatment of cancer resistance.Frontiers in cell and developmental biology · 2023Review
- Stimulation of soluble guanylate cyclase by vericiguat reduces skeletal muscle atrophy of mice following chemotherapy.Frontiers in pharmacology · 2023Article
- Article
- Chemotherapeutic drug screening in 3D-Bioengineered human myobundles provides insight into taxane-induced myotoxicities.iScience · 2022Article
- Article
- Low-level laser prevents doxorubicin-induced skeletal muscle atrophy by modulating AMPK/SIRT1/PCG-1α-mediated mitochondrial function, apoptosis and up-regulation of pro-inflammatory responses.Cell & bioscience · 2021Article
- Review
- Phenotypic features of cancer cachexia-related loss of skeletal muscle mass and function: lessons from human and animal studies.Journal of cachexia, sarcopenia and muscle · 2021Review
- Consideration of Sex as a Biological Variable in the Development of Doxorubicin Myotoxicity and the Efficacy of Exercise as a Therapeutic Intervention.Antioxidants (Basel, Switzerland) · 2021Review
- Skeletal Muscle Deconditioning in Breast Cancer Patients Undergoing Chemotherapy: Current Knowledge and Insights From Other Cancers.Frontiers in cell and developmental biology · 2021Review
- EO771, is it a well-characterized cell line for mouse mammary cancer model? Limit and uncertainty.Cancer medicine · 2020Review
- Neutralizing mitochondrial ROS does not rescue muscle atrophy induced by hindlimb unloading in female mice.Journal of applied physiology (Bethesda, Md. : 1985) · 2020Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
The loss of strength in combination with constant fatigue is a burden on cancer patients undergoing chemotherapy. Doxorubicin, a standard chemotherapy drug used in the clinic, causes skeletal muscle dysfunction and increases mitochondrial H2O2 We hypothesized that the combined effect of cancer and chemotherapy in an immunocompetent breast cancer mouse model (E0771) would compromise skeletal muscle mitochondrial respiratory function, leading to an increase in H2O2-emitting potential and impaired muscle function. Here, we demonstrate that cancer chemotherapy decreases mitochondrial respiratory capacity supported with complex I (pyruvate/glutamate/malate) and complex II (succinate) substrates. Mitochondrial H2O2-emitting potential was altered in skeletal muscle, and global protein oxidation was elevated with cancer chemotherapy. Muscle contractile function was impaired following exposure to cancer chemotherapy. Genetically engineering the overexpression of catalase in mitochondria of muscle attenuated mitochondrial H2O2 emission and protein oxidation, preserving mitochondrial and whole muscle function despite cancer chemotherapy. These findings suggest mitochondrial oxidants as a mediator of cancer chemotherapy-induced skeletal muscle dysfunction.
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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.