ArticlePloS one2012
Increase in muscle mitochondrial biogenesis does not prevent muscle loss but increased tumor size in a mouse model of acute cancer-induced cachexia.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
28 citing papers in PubMed, 52 citations in OpenAlex.
- Role of mitochondrial dysfunction in muscle wasting in cancer cachexia: a narrative review.Journal of translational medicine · 2026Review
- Vascular collapse leads to muscle wasting in cancer cachexia.Nature cancer · 2025Article
- AMPK as a mediator of tissue preservation: time for a shift in dogma?Nature reviews. Endocrinology · 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
- Effects of Monoamino-Oxidase-A (MAO-A) Inhibition on Skeletal Muscle Inflammation and Wasting through Pancreatic Ductal Adenocarcinoma in Triple Transgenic Mice.Biomedicines · 2023Article
- Targeting Mitochondria and Oxidative Stress in Cancer- and Chemotherapy-Induced Muscle Wasting.Antioxidants & redox signaling · 2023Review
- Impact of cancer cachexia on respiratory muscle function and the therapeutic potential of exercise.The Journal of physiology · 2022Review
- PGC1α overexpression preserves muscle mass and function in cisplatin-induced cachexia.Journal of cachexia, sarcopenia and muscle · 2022Article
- PGC-1α overexpression is not sufficient to mitigate cancer cachexia in either male or female mice.Applied physiology, nutrition, and metabolism = Physiologie appliquee, nutrition et metabolisme · 2022Article
- Cardiac Remodeling in Cancer-Induced Cachexia: Functional, Structural, and Metabolic Contributors.Cells · 2022Review
- Review
- Shared and distinct mechanisms of skeletal muscle atrophy: A narrative review.Ageing research reviews · 2021Review
- Metabolic Remodeling in Skeletal Muscle Atrophy as a Therapeutic Target.Metabolites · 2021Review
- Voluntary exercise prevents abnormal muscle mitochondrial morphology in cancer cachexia mice.Physiological reports · 2021Article
- Mitochondrial Dysfunction Is a Common Denominator Linking Skeletal Muscle Wasting Due to Disease, Aging, and Prolonged Inactivity.Antioxidants (Basel, Switzerland) · 2021Review
- Muscle alterations in the development and progression of cancer-induced muscle atrophy: a review.Journal of applied physiology (Bethesda, Md. : 1985) · 2020Review
- High-Frequency Stimulation on Skeletal Muscle Maintenance in Female Cachectic Mice.Medicine and science in sports and exercise · 2019Article
- Isoform-specific role of Na/K-ATPase α1 in skeletal muscle.American journal of physiology. Endocrinology and metabolism · 2018Article
- Modulating Metabolism to Improve Cancer-Induced Muscle Wasting.Oxidative medicine and cellular longevity · 2018Review
- Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Cancer-associated cachexia is a complex metabolic condition characterized by the progressive loss of body fat and deterioration of muscle mass. Although the cellular and molecular mechanisms of cachexia are incompletely understood, previous studies have suggested mitochondrial dysfunction in murine models of cancer cachexia. To better understand the metabolic shift in cancer-induced cachexia, we studied the effects of enhanced oxidative capacity on muscle wasting using transgenic mice over-expressing Peroxisome Proliferator-Activated Receptor gamma Co-activator-1α (PGC-1α) in skeletal muscle in a Lewis lung carcinoma-implanted model. Increased mitochondrial biogenesis was observed in the skeletal muscle of tumor-implanted mice. However, these increases did not prevent or reverse muscle wasting in mice harboring tumors. Moreover, tumor size was increased in muscle PGC-1α over-expressing mice. We found similar levels of circulating inflammatory cytokines in tumor-implanted animals, which was not affected by increased muscle expression of PGC-1α. Our data indicated that increased mitochondrial biogenesis in skeletal muscle is not sufficient to rescue tumor-associated, acute muscle loss, and could promote tumor growth, possibly through the release of myokines.
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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.