ReviewClinical and experimental nephrology2013
Mechanisms stimulating muscle wasting in chronic kidney disease: the roles of the ubiquitin-proteasome system and myostatin.
Review in Clinical and experimental nephrology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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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.
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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
29 citing papers in PubMed, 53 citations in OpenAlex.
- Review
- Research trends and potential molecular intersections between diabetic kidney disease and sarcopenia: a 21-year bibliometric and bioinformatics analysis.Frontiers in endocrinology · 2026Review
- Exploring genetic association of chronic kidney disease with sarcopenia among European population: a bidirectional Mendelian randomization study.Clinical and experimental nephrology · 2025Article
- Interplay between Skeletal Muscle Catabolism and Remodeling of Arteriovenous Fistula by Yes-Associated Protein 1 (YAP1) Signaling.Journal of the American Society of Nephrology : JASN · 2025Article
- The roles of the ubiquitin-proteasome system in renal disease.International journal of medical sciences · 2025Review
- Review of Exercise Interventions to Improve Clinical Outcomes in Nondialysis CKD.Kidney international reports · 2024Review
- Inflammatory Cytokine-Induced Muscle Atrophy and Weakness Can Be Ameliorated by an Inhibition of TGF-β-Activated Kinase-1.International journal of molecular sciences · 2024Article
- A tryptophan-derived uremic metabolite/Ahr/Pdk4 axis governs skeletal muscle mitochondrial energetics in chronic kidney disease.JCI insight · 2024Article
- Exercise for patients with chronic kidney disease: from cells to systems to function.American journal of physiology. Renal physiology · 2024Review
- Correlation between serum trimethylamine-Renal failure · 2022Article
- Muscle Wasting in Chronic Kidney Disease: Mechanism and Clinical Implications-A Narrative Review.International journal of molecular sciences · 2022Review
- Article
- Skeletal myopathy in CKD: a comparison of adenine-induced nephropathy and 5/6 nephrectomy models in mice.American journal of physiology. Renal physiology · 2021Article
- Tissue-SpecificMetabolites · 2021Article
- Uremic metabolites impair skeletal muscle mitochondrial energetics through disruption of the electron transport system and matrix dehydrogenase activity.American journal of physiology. Cell physiology · 2019Article
- Myostatin regulates pituitary development and hepatic IGF1.American journal of physiology. Endocrinology and metabolism · 2019Article
- Chronic kidney disease: considerations for monitoring skeletal muscle health and prescribing resistance exercise.Clinical kidney journal · 2018Article
- Association of Uremic Toxins and Inflammatory Markers with Physical Performance in Dialysis Patients.Toxins · 2018Observational
- Chronic kidney disease progression: a retrospective analysis of 3-year adherence to a low protein diet.Renal failure · 2017Article
- Associations Between Low Serum Testosterone and All-Cause Mortality and Infection-Related Hospitalization in Male Hemodialysis Patients: A Prospective Cohort Study.Kidney international reports · 2017Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Catabolic conditions including chronic kidney disease (CKD), cancer, and diabetes cause muscle atrophy. The loss of muscle mass worsens the burden of disease because it is associated with increased morbidity and mortality. To avoid these problems or to develop treatment strategies, the mechanisms leading to muscle wasting must be identified. Specific mechanisms uncovered in CKD generally occur in other catabolic conditions. These include stimulation of protein degradation in muscle arising from activation of caspase-3 and the ubiquitin-proteasome system (UPS). These proteases act in a coordinated fashion with caspase-3 initially cleaving the complex structure of proteins in muscle, yielding fragments that are substrates that are degraded by the UPS. Fortunately, the UPS exhibits remarkable specificity for proteins to be degraded because it is the major intracellular proteolytic system. Without a high level of specificity cellular functions would be disrupted. The specificity is accomplished by complex reactions that depend on recognition of a protein substrate by specific E3 ubiquitin ligases. In muscle, the specific ligases are Atrogin-1 and MuRF-1, and their expression has characteristics of a biomarker of accelerated muscle proteolysis. Specific complications of CKD (metabolic acidosis, insulin resistance, inflammation, and angiotensin II) activate caspase-3 and the UPS through mechanisms that include glucocorticoids and impaired insulin or IGF-1 signaling. Mediators activate myostatin, which functions as a negative growth factor in muscle. In models of cancer or CKD, strategies that block myostatin prevent muscle wasting, suggesting that therapies that block myostatin could prevent muscle wasting in catabolic conditions.
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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.