ReviewMolecules (Basel, Switzerland)2021
Ubiquitin Ligases at the Heart of Skeletal Muscle Atrophy Control.
Review in Molecules (Basel, Switzerland), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
45 citing papers in PubMed, 1 synthesis or guideline pooled it, 78 citations in OpenAlex.
- Biomarkers of Skeletal Muscle Atrophy Based on Atrogenes Evaluation: A Systematic Review and Meta-Analysis Study.International journal of molecular sciences · 2025Pooled it
- The Secretome of a Cachexia-Inducing Lung Tumor Impairs Mitochondrial Function and Skeletal Muscle Differentiation.Cancers · 2026Article
- JAK1/2 inhibitor ruxolitinib reduces aggregates in cardiac proteinopathy.EMBO molecular medicine · 2026Article
- Tumor-muscle communication in cancer-associated cachexia (Review).Oncology letters · 2026Review
- Effects and Molecular Mechanisms of Heat-Killed PostbioticInternational journal of molecular sciences · 2026Article
- Mitochondrial ROS dyshomeostasis: a key driver of accelerated supraspinatus atrophy after rotator cuff injury.Frontiers in physiology · 2026Review
- Elevated circulating GDF11 and its role in age-related sarcopenia: insights from clinical, transcriptomic, andFrontiers in aging · 2026Article
- Umbilical cord mesenchymal stromal cells in sarcopenia: benefits and strategies for enhancing efficacy.Stem cell research & therapy · 2025Review
- Physical Activity, Exerkines, and Their Role in Cancer Cachexia.International journal of molecular sciences · 2025Review
- P-Coumaric Acid Improves Skeletal Muscle Atrophy in Chronic Kidney Disease by Modulating TLR4/MyD88/NF-κB-Mediated Inflammation and Oxidative Stress.Journal of cellular and molecular medicine · 2025Article
- Analyses of Off-Target Effects on Cardiac and Skeletal Muscles by Berberine, a Drug Used to Treat Cancers and Induce Weight Loss.Cytoskeleton (Hoboken, N.J.) · 2025Article
- Associations between sedentary behaviour and sarcopenia among patients aged 40 and older with chronic obstructive pulmonary disease: a cross-sectional study.BMC public health · 2025Article
- CCL5 Induces a Sarcopenic-like Phenotype via the CCR5 Receptor.Antioxidants (Basel, Switzerland) · 2025Article
- Impact of exercise-induced DNA damage repair on age-related muscle weakness and sarcopenia.Frontiers in genetics · 2025Review
- The gut-muscle axis: a comprehensive review of the interplay between physical activity and gut microbiota in the prevention and treatment of muscle wasting disorders.Frontiers in microbiology · 2025Review
- Identification of key modules and hub genes for sepsis-induced myopathy using weighted gene co-expression network analysis.Frontiers in genetics · 2025Article
- A novel short-course, low-intensity blood-flow-restricted exercise (BFRE) regimen to study satellite cell function in critical illness survivors with sustained muscle atrophy following intensive care unit-acquired weakness (ICUAW).Frontiers in physiology · 2025Article
- Targeting MuRF1 to Combat Skeletal Muscle Wasting in Cardiac Cachexia: Mechanisms and Therapeutic Prospects.Medical science monitor : international medical journal of experimental and clinical research · 2024Review
- Ubiquitination Insight from Spinal Muscular Atrophy-From Pathogenesis to Therapy: A Muscle Perspective.International journal of molecular sciences · 2024Review
- Deubiquitinases in muscle physiology and disorders.Biochemical Society transactions · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Skeletal muscle loss is a detrimental side-effect of numerous chronic diseases that dramatically increases mortality and morbidity. The alteration of protein homeostasis is generally due to increased protein breakdown while, protein synthesis may also be down-regulated. The ubiquitin proteasome system (UPS) is a master regulator of skeletal muscle that impacts muscle contractile properties and metabolism through multiple levers like signaling pathways, contractile apparatus degradation, etc. Among the different actors of the UPS, the E3 ubiquitin ligases specifically target key proteins for either degradation or activity modulation, thus controlling both pro-anabolic or pro-catabolic factors. The atrogenes MuRF1/TRIM63 and MAFbx/Atrogin-1 encode for key E3 ligases that target contractile proteins and key actors of protein synthesis respectively. However, several other E3 ligases are involved upstream in the atrophy program, from signal transduction control to modulation of energy balance. Controlling E3 ligases activity is thus a tempting approach for preserving muscle mass. While indirect modulation of E3 ligases may prove beneficial in some situations of muscle atrophy, some drugs directly inhibiting their activity have started to appear. This review summarizes the main signaling pathways involved in muscle atrophy and the E3 ligases implicated, but also the molecules potentially usable for future therapies.
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What Socratic holds
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 Socratic graph.