ArticleInternational journal of molecular sciences2020
Mitochondrial Function and Protein Turnover in the Diaphragm are Altered in LLC Tumor Model of Cancer Cachexia.
Article in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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The trial behind it
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Who cites it
12 citing papers in PubMed, 14 citations in OpenAlex.
- The Secretome of a Cachexia-Inducing Lung Tumor Impairs Mitochondrial Function and Skeletal Muscle Differentiation.Cancers · 2026Article
- Tumour-driven lipid accumulation in oenocytes reflects systemic lipid alterations.PLoS genetics · 2026Article
- Pharmacokinetic Implications of Pathophysiological Changes in Cachexia Syndrome: A Scoping Review.European journal of drug metabolism and pharmacokinetics · 2025Article
- GL261 glioblastoma induces delayed body weight gain and stunted skeletal muscle growth in young mice.American journal of physiology. Regulatory, integrative and comparative physiology · 2025Article
- Exploring heterogeneity: a dive into preclinical models of cancer cachexia.American journal of physiology. Cell physiology · 2024Review
- Immunoregulation in cancer-associated cachexia.Journal of advanced research · 2024Review
- Effects of Monoamino-Oxidase-A (MAO-A) Inhibition on Skeletal Muscle Inflammation and Wasting through Pancreatic Ductal Adenocarcinoma in Triple Transgenic Mice.Biomedicines · 2023Article
- Muscle weakness precedes atrophy during cancer cachexia and is linked to muscle-specific mitochondrial stress.JCI insight · 2022Article
- Impact of cancer cachexia on respiratory muscle function and the therapeutic potential of exercise.The Journal of physiology · 2022Review
- Cancer cachexia as a multiorgan failure: Reconstruction of the crime scene.Frontiers in cell and developmental biology · 2022Review
- Review
- Mitochondrial Dysfunction Is a Common Denominator Linking Skeletal Muscle Wasting Due to Disease, Aging, and Prolonged Inactivity.Antioxidants (Basel, Switzerland) · 2021Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
It is established that cancer cachexia causes limb muscle atrophy and is strongly associated with morbidity and mortality; less is known about how the development of cachexia impacts the diaphragm. The purpose of this study was to investigate cellular signaling mechanisms related to mitochondrial function, reactive oxygen species (ROS) production, and protein synthesis during the development of cancer cachexia. C57BL/J6 mice developed Lewis Lung Carcinoma for either 0 weeks (Control), 1 week, 2 weeks, 3 weeks, or 4 weeks. At designated time points, diaphragms were harvested and analyzed. Mitochondrial respiratory control ratio was ~50% lower in experimental groups, which was significant by 2 weeks of cancer development, with no difference in mitochondrial content markers COXIV or VDAC. Compared to the controls, ROS was 4-fold elevated in 2-week animals but then was not different at later time points. Only one antioxidant protein, GPX3, was altered by cancer development (~70% lower in experimental groups). Protein synthesis, measured by a fractional synthesis rate, appeared to become progressively lower with the cancer duration, but the mean difference was not significant. The development and progression of cancer cachexia induces marked alterations to mitochondrial function and ROS production in the diaphragm and may contribute to increased cachexia-associated morbidity and mortality.
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Registered trials
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