ReviewBiomolecules2021
Out of Control: The Role of the Ubiquitin Proteasome System in Skeletal Muscle during Inflammation.
Review in Biomolecules, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT07017517 (Effect of Physical Therapy on NLRP3 Inflammasome Activation and Muscle Atrophy in Critical Illness Myopathy), which is not on this map. Cited by 63 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.
Effect of Physical Therapy on NLRP3 Inflammasome Activation and Muscle Atrophy in Critical Illness Myopathy (PT-NLRP3-CIM).
Who cites it
63 citing papers in PubMed, 1 synthesis or guideline pooled it, 89 citations in OpenAlex.
- Evidence that tirzepatide protects against diabetes-related cardiac damages.Cardiovascular diabetology · 2024 · on this mapPooled it
- Shared mechanisms of musculoskeletal dysfunction in type 2 diabetes mellitus: Insights into future therapeutic directions (Review).International journal of molecular medicine · 2026Review
- Review
- Muscle Dysfunction in Critical Illness: Established Mechanisms and the Potential Contribution of the NLRP3 Inflammasome.International journal of molecular sciences · 2026Review
- Sarcopenia and Frailty in COPD: Mechanisms, Relationship with Malnutrition and Potential Therapeutic Interventions.Nutrients · 2026Review
- Exercise-induced modulation of the unfolded protein response: a therapeutic avenue for muscle wasting disorders.Journal of physiology and biochemistry · 2026Review
- Article
- Multi-Axis Reprogramming of Muscle-Metabolic Crosstalk by HiLo Platinum™ Restores Strength in Prediabetes via Mitochondrial Activation and Gut Microbiome Remodeling.International journal of molecular sciences · 2026Article
- Short-chain fatty acids alleviate sarcopenia in rats via modulation of the NF-κB signaling pathway.Scientific reports · 2026Article
- Parthenolide Attenuates Skeletal Muscle Atrophy Through Regulation of Protein Homeostasis and Inhibition of Inflammation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Research progress on the molecular mechanism and clinical evidence of glucagon-like peptide-1 receptor agonists in improving sarcopenia.Diabetology & metabolic syndrome · 2026Review
- Article
- Transcriptional Adaptations to Muscle Loading in a Murine Model of Achilles Tendinopathy.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2026Article
- Sepsis-associated skeletal muscle wasting is ameliorated by pharmacological inhibition of the STAT3 signaling pathway in mice.Scientific reports · 2026Article
- Composite dietary fiber alleviates obesity-induced skeletal muscle atrophy by regulating gut microbiota-derived short-chain fatty acids in mice.NPJ science of food · 2026Article
- Beyond muscle weakness: pathogenesis of sepsis-induced myopathy and its management.Open medicine (Warsaw, Poland) · 2026Review
- Traditional Chinese Medicine for Diabetic Sarcopenia: A Review and Its Related Mechanisms.Journal of diabetes research · 2026Review
- Mitochondrial ROS dyshomeostasis: a key driver of accelerated supraspinatus atrophy after rotator cuff injury.Frontiers in physiology · 2026Review
- Sarcopenia and sepsis fuel a self-perpetuating cycle of immunometabolism decline.Frontiers in immunology · 2026Review
- Branched-chain amino acids and sepsis: from pathological mechanisms to clinical interventions.Nutrition & metabolism · 2025Review
3 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The majority of critically ill intensive care unit (ICU) patients with severe sepsis develop ICU-acquired weakness (ICUAW) characterized by loss of muscle mass, reduction in myofiber size and decreased muscle strength leading to persisting physical impairment. This phenotype results from a dysregulated protein homeostasis with increased protein degradation and decreased protein synthesis, eventually causing a decrease in muscle structural proteins. The ubiquitin proteasome system (UPS) is the predominant protein-degrading system in muscle that is activated during diverse muscle atrophy conditions, e.g., inflammation. The specificity of UPS-mediated protein degradation is assured by E3 ubiquitin ligases, such as atrogin-1 and MuRF1, which target structural and contractile proteins, proteins involved in energy metabolism and transcription factors for UPS-dependent degradation. Although the regulation of activity and function of E3 ubiquitin ligases in inflammation-induced muscle atrophy is well perceived, the contribution of the proteasome to muscle atrophy during inflammation is still elusive. During inflammation, a shift from standard- to immunoproteasome was described; however, to which extent this contributes to muscle wasting and whether this changes targeting of specific muscular proteins is not well described. This review summarizes the function of the main proinflammatory cytokines and acute phase response proteins and their signaling pathways in inflammation-induced muscle atrophy with a focus on UPS-mediated protein degradation in muscle during sepsis. The regulation and target-specificity of the main E3 ubiquitin ligases in muscle atrophy and their mode of action on myofibrillar proteins will be reported. The function of the standard- and immunoproteasome in inflammation-induced muscle atrophy will be described and the effects of proteasome-inhibitors as treatment strategies will be discussed.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.