ArticleJournal of cachexia, sarcopenia and muscle2016
Cancer cachexia causes skeletal muscle damage via transient receptor potential vanilloid 2-independent mechanisms, unlike muscular dystrophy.
Article in Journal of cachexia, sarcopenia and muscle, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 28 citations in OpenAlex.
- Calcium and TRPML-Mediated Autophagy: Implications in Cancer, Cardiovascular Diseases, and Cardio-Oncology.Cardiovascular toxicology · 2026Review
- The role and mechanisms of myokines in sarcopenia: new intervention strategies for the challenges of aging.Frontiers in medicine · 2025Review
- Serum creatine kinase elevation following tyrosine kinase inhibitor treatment in cancer patients: Symptoms, mechanism, and clinical management.Clinical and translational science · 2024Review
- Embryo thermal manipulation enhances mitochondrial function in the skeletal muscle of heat-stressed broilers by regulating transient receptor potential V2 expression.Poultry science · 2024Article
- Signaling roles of platelets in skeletal muscle regeneration.BioEssays : news and reviews in molecular, cellular and developmental biology · 2023Article
- Platelet-derived chemokines promote skeletal muscle regeneration by guiding neutrophil recruitment to injured muscles.Nature communications · 2023Article
- The myokine Fibcd1 is an endogenous determinant of myofiber size and mitigates cancer-induced myofiber atrophy.Nature communications · 2022Article
- REDD1 deletion attenuates cancer cachexia in mice.Journal of applied physiology (Bethesda, Md. : 1985) · 2021Article
- Activated mast cells in skeletal muscle can be a potential mediator for cancer-associated cachexia.Journal of cachexia, sarcopenia and muscle · 2021Article
- Surface-directed engineering of tissue anisotropy in microphysiological models of musculoskeletal tissue.Science advances · 2021Article
- Article
- Hepatic alterations during the development and progression of cancer cachexia.Applied physiology, nutrition, and metabolism = Physiologie appliquee, nutrition et metabolisme · 2020Article
- The TRPV2 cation channels: from urothelial cancer invasiveness to glioblastoma multiforme interactome signature.Laboratory investigation; a journal of technical methods and pathology · 2020Review
- Blockade of TRPV2 is a Novel Therapy for Cardiomyopathy in Muscular Dystrophy.International journal of molecular sciences · 2019Review
- Metabolic disorders in heart failure and cancer.ESC heart failure · 2018Review
- Contemporary publication patterns in the Journal of Cachexia, Sarcopenia and Muscle by type and sub-speciality: facts and numbers.Journal of cachexia, sarcopenia and muscle · 2018Article
- Muscle regeneration is disrupted by cancer cachexia without loss of muscle stem cell potential.PloS one · 2018Article
- The mitochondrial metabolic reprogramming agent trimetazidine as an 'exercise mimetic' in cachectic C26-bearing mice.Journal of cachexia, sarcopenia and muscle · 2017Article
- Understanding tumor anabolism and patient catabolism in cancer-associated cachexia.American journal of cancer research · 2017Article
- Cancer cachexia causes skeletal muscle damage via transient receptor potential vanilloid 2-independent mechanisms, unlike muscular dystrophy.Journal of cachexia, sarcopenia and muscle · 2016Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMuscle wasting during cancer cachexia contributes to patient morbidity. Cachexia-induced muscle damage may be understood by comparing its symptoms with those of other skeletal muscle diseases, but currently available data are limited.
methodsWe modelled cancer cachexia in mice bearing Lewis lung carcinoma/colon adenocarcinoma and compared the associated muscle damage with that in a murine muscular dystrophy model (mdx mice). We measured biochemical and immunochemical parameters: amounts/localization of cytoskeletal proteins and/or Ca(2+) signalling proteins related to muscle function and abnormality. We analysed intracellular Ca(2+) mobilization and compared results between the two models. Involvement of Ca(2+)-permeable channel transient receptor potential vanilloid 2 (TRPV2) was examined by inoculating Lewis lung carcinoma cells into transgenic mice expressing dominant-negative TRPV2.
resultsTumourigenesis caused loss of body and skeletal muscle weight and reduced muscle force and locomotor activity. Similar to mdx mice, cachexia muscles exhibited myolysis, reduced sarcolemmal sialic acid content, and enhanced lysosomal exocytosis and sarcolemmal localization of phosphorylated Ca(2+)/CaMKII. Abnormal autophagy and degradation of dystrophin also occurred. Unlike mdx muscles, cachexia muscles did not exhibit regeneration markers (centrally nucleated fibres), and levels of autophagic proteolytic pathway markers increased. While a slight accumulation of TRPV2 was observed in cachexia muscles, Ca(2+) influx via TRPV2 was not elevated in cachexia-associated myotubes, and the course of cachexia pathology was not ameliorated by dominant-negative inhibition of TRPV2.
conclusionsThus, cancer cachexia may induce muscle damage through TRPV2-independent mechanisms distinct from those in muscular dystrophy; this may help treat patients with tumour-induced muscle wasting.
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