ReviewThe Journal of biological chemistry2026
Mechanisms of protein degradation in atrophying muscles: What have we learned during the past decade?
Review in The Journal of biological chemistry, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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
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
7 citing papers in PubMed.
- FBXL21 regulates diurnal proteostasis in skeletal muscle by targeting DNAJB6 and client proteins.EMBO reports · 2026Article
- Interactions Between E3 Ubiquitin Ligases and Deubiquitinases in AKT Regulation: Implications in Skeletal Muscle Homeostasis.Cell biochemistry and function · 2026Review
- Effects of variable incubation temperature during embryonic days 10-13 on leg muscle transcriptomics in day-old broiler and layer chicks.Scientific reports · 2026Article
- Skeletal muscle adaptation to microgravity: how altered mechanical cues drive catabolic signaling.EMBO reports · 2026Review
- Article
- FBXL21 regulates diurnal proteostasis and stress response by targeting DNAJB6 and client proteins.bioRxiv : the preprint server for biology · 2026Article
- Neutrophil percentage-to-albumin ratio is associated with low muscle mass risk in rheumatoid arthritis: evidence from a hospital-based cohort and NHANES validation.Frontiers in immunology · 2026Article
Corrections and comments
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Authors and funding
1 author.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Skeletal muscle atrophy occurs in diverse conditions, including aging, disuse, cancer cachexia, and chronic disease. It results from an imbalance between protein synthesis and degradation, where excessive proteolysis drives loss of contractile proteins, weakness, and metabolic decline. Recent advances in structural biology, multi-omics approaches, and high-resolution imaging have uncovered how sarcomeric and cytoskeletal components are gradually degraded by ubiquitin ligases, proteasomes, and autophagy. Mechanical loading and mechanotransduction emerge as key regulators of proteostasis, linking tension to anabolic signaling. Transcriptional and epigenetic control through IGF1-Akt-mTOR, TGF-β, inflammatory cytokines, and circadian rhythms, as well as non-coding RNAs and miRNAs, also contribute to wasting. This review summarizes these recent findings and novel therapeutic strategies, such as restoring mitochondrial function and modulating RNA networks and mechanosensitive signaling to preserve muscle mass and function.
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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 Socratic graph.