ReviewJournal of muscle research and cell motility2015
Skeletal muscle atrophy: disease-induced mechanisms may mask disuse atrophy.
Review in Journal of muscle research and cell motility, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.
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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
36 citing papers in PubMed, 1 synthesis or guideline pooled it, 60 citations in OpenAlex.
- Doxorubicin-induced skeletal muscle atrophy: Elucidating the underlying molecular pathways.Acta physiologica (Oxford, England) · 2020Pooled it
- How Acute and Chronic Exercise Regulate Muscle Atrophic Genes to Mitigate Sarcopenia: A Narrative Review.Sports medicine (Auckland, N.Z.) · 2026Review
- Exercise mitigates IL-27-induced muscle atrophy following myocardial infarction through anti-inflammatory mechanisms.Journal of translational medicine · 2026Article
- Article
- Combating chronic kidney disease-associated cachexia: A literature review of recent therapeutic approaches.BMC nephrology · 2025Review
- Transcriptomic adaptation of skeletal muscle in response to MICT and HIIT exercise modalities.PloS one · 2025Article
- Myotendinous junction: a microenvironment favorable for short-term adaptations to resistance training following gastrocnemius muscle atrophy.Frontiers in physiology · 2025Article
- Lumbrical muscle enhancement on MRI and its association with rheumatoid arthritis.Skeletal radiology · 2023Article
- The long-term impact of the COVID-19 pandemic on physical fitness in young adults: a historical control study.Scientific reports · 2023Article
- Gut microbiota in muscular atrophy development, progression, and treatment: New therapeutic targets and opportunities.Innovation (Cambridge (Mass.)) · 2023Review
- Article
- Division of loading time in reloading the disused atrophic soleus muscle induces proximal muscle injury.Journal of physical therapy science · 2023Article
- Predictors of muscle hypertrophy responsiveness to electrically evoked resistance training after spinal cord injury.European journal of applied physiology · 2023Article
- The Role of Skeletal Muscle Mitochondria in Colorectal Cancer Related Cachexia: Friends or Foes?International journal of molecular sciences · 2022Review
- Effect of CLife (Basel, Switzerland) · 2022Article
- Oyster Hydrolysates Attenuate Muscle Atrophy via Regulating Protein Turnover and Mitochondria Biogenesis in C2C12 Cell and Immobilized Mice.Nutrients · 2021Article
- Integration of proteomic and genetic approaches to assess developmental muscle atrophy.The Journal of experimental biology · 2021Article
- Genetic variability affects the response of skeletal muscle to disuse.Journal of musculoskeletal & neuronal interactions · 2021Article
- Article
- Angiotensin II-induced muscle atrophy via PPARγ suppression is mediated by miR-29b.Molecular therapy. Nucleic acids · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Disuse atrophy is the loss of skeletal muscle mass due to inactivity or lower than 'normal' use. It is not only a furtive component of the 'modern' sedentary lifestyle but also a part of numerous pathologies, where muscle loss is linked to disease specific and/or other toxicity factors, eventually leading to wasting (cachexia). Whether disuse-or-disease induced, muscle loss leads to weakness and metabolic comorbidities with a high societal and financial cost. This review discusses the intricate network of interacting signalling pathways including Atrogin-1/MAFbx, IGF1-Akt, myostatin, glucocorticoids, NF-kB, MAPKs and caspases that seem to regulate disuse atrophy but also share common activation patterns in other states of muscle loss such as sarcopenia or cachexia. Reactive oxygen species are also important regulators of cell signalling pathways that can accelerate proteolysis and depress protein synthesis. Exercise is an effective countermeasure and antioxidants may show some benefit. We discuss how the experimental model used can crucially affect the outcome and hence our understanding of atrophy. Timing of sampling is crucial as some signalling mechanisms reach their peak early during the atrophy process to rapidly decline thereafter, while other present high levels even weeks and months after study initiation. The importance of such differences lays in future consideration of appropriate treatment targets. Apart from attempting to correct defective genes or negate their effects, technological advances in new rational ways should aim to regulate specific gene expression at precise time points for the treatment of muscle atrophy in therapeutic protocols depending on the origin of atrophy induction.
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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.