ArticleJournal of cachexia, sarcopenia and muscle2020
Cancer cachexia in a mouse model of oxidative stress.
Article in Journal of cachexia, sarcopenia and muscle, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 52 citations in OpenAlex.
- PEBP4 alleviates muscle wasting in lung cancer cachexia via KEAP1-NRF2-mediated redox homeostasis.Cell death & disease · 2026Article
- Loss of calcium-dependent phospholipase A2 contributes to multi-omic changes in mouse denervated skeletal muscle.Physiological reports · 2026Article
- Unacylated ghrelin counteracts mitochondrial dysfunction and neuromuscular junction disruption in cancer cachexia.American journal of physiology. Cell physiology · 2026Article
- Phospholipid Glutathione Peroxidase Overexpression Mitigates Cancer Cachexia by Protecting Muscle Mass and Lowering Inflammation.Journal of cachexia, sarcopenia and muscle · 2026Article
- Vitamin B1 Involved inInternational journal of molecular sciences · 2025Article
- Nuciferine Attenuates Cancer Cachexia-Induced Muscle Wasting in Mice via HSP90AA1.Journal of cachexia, sarcopenia and muscle · 2025Article
- Pharmacological reduction of lipid hydroperoxides as a potential modulator of sarcopenia.The Journal of physiology · 2025Article
- Article
- Limiting serine availability during tumor progression promotes muscle wasting in cancer cachexia.Cell death discovery · 2024Article
- Tumour-induced alterations in single-nucleus transcriptome of atrophying muscles indicate enhanced protein degradation and reduced oxidative metabolism.Journal of cachexia, sarcopenia and muscle · 2024Article
- Exploring heterogeneity: a dive into preclinical models of cancer cachexia.American journal of physiology. Cell physiology · 2024Review
- Preventing loss of sirt1 lowers mitochondrial oxidative stress and preserves C2C12 myotube diameter in an in vitro model of cancer cachexia.Physiological reports · 2024Article
- Senolytic treatment does not mitigate oxidative stress-induced muscle atrophy but improves muscle force generation in CuZn superoxide dismutase knockout mice.GeroScience · 2024Article
- Lipid-Lowering Medications are Associated with Reduced Sarcopenia-Related Quality of Life in Older Adults with Hyperlipidemia.Drugs & aging · 2024Article
- Transcriptome-based deep learning analysis identifies drug candidates targeting protein synthesis and autophagy for the treatment of muscle wasting disorder.Experimental & molecular medicine · 2024Article
- Long-term Musculoskeletal Consequences of Chemotherapy in Pediatric Mice.Function (Oxford, England) · 2024Article
- Article
- Modulation of sarcopenia phenotypes by glutathione peroxidase 4 overexpression in mice.The Journal of physiology · 2023Article
- Muscle p62 stimulates the expression of antioxidant proteins alleviating cancer cachexia.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2023Article
- Skeletal and cardiac muscle have different protein turnover responses in a model of right heart failure.GeroScience · 2023Article
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Authors and funding
15 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundCancer is associated with muscle atrophy (cancer cachexia) that is linked to up to 40% of cancer-related deaths. Oxidative stress is a critical player in the induction and progression of age-related loss of muscle mass and weakness (sarcopenia); however, the role of oxidative stress in cancer cachexia has not been defined. The purpose of this study was to examine if elevated oxidative stress exacerbates cancer cachexia.
methodsCu/Zn superoxide dismutase knockout (Sod1KO) mice were used as an established mouse model of elevated oxidative stress. Cancer cachexia was induced by injection of one million Lewis lung carcinoma (LLC) cells or phosphate-buffered saline (saline) into the hind flank of female wild-type mice or Sod1KO mice at approximately 4 months of age. The tumour developed for 3 weeks. Muscle mass, contractile function, neuromuscular junction (NMJ) fragmentation, metabolic proteins, mitochondrial function, and motor neuron function were measured in wild-type and Sod1KO saline and tumour-bearing mice. Data were analysed by two-way ANOVA with Tukey-Kramer post hoc test when significant F ratios were determined and α was set at 0.05. Unless otherwise noted, results in abstract are mean ±SEM.
resultsMuscle mass and cross-sectional area were significantly reduced, in tumour-bearing mice. Metabolic enzymes were dysregulated in Sod1KO mice and cancer exacerbated this phenotype. NMJ fragmentation was exacerbated in tumour-bearing Sod1KO mice. Myofibrillar protein degradation increased in tumour-bearing wild-type mice (wild-type saline, 0.00847 ± 0.00205; wildtype LLC, 0.0211 ± 0.00184) and tumour-bearing Sod1KO mice (Sod1KO saline, 0.0180 ± 0.00118; Sod1KO LLC, 0.0490 ± 0.00132). Muscle mitochondrial oxygen consumption was reduced in tumour-bearing mice compared with saline-injected wild-type mice. Mitochondrial protein degradation increased in tumour-bearing wild-type mice (wild-type saline, 0.0204 ± 0.00159; wild-type LLC, 0.167 ± 0.00157) and tumour-bearing Sod1KO mice (Sod1KO saline, 0.0231 ± 0.00108; Sod1 KO LLC, 0.0645 ± 0.000631). Sciatic nerve conduction velocity was decreased in tumour-bearing wild-type mice (wild-type saline, 38.2 ± 0.861; wild-type LLC, 28.8 ± 0.772). Three out of eleven of the tumour-bearing Sod1KO mice did not survive the 3-week period following tumour implantation.
conclusionsOxidative stress does not exacerbate cancer-induced muscle loss; however, cancer cachexia may accelerate NMJ disruption.
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