ArticleShock (Augusta, Ga.)2017
Restorative Mechanisms Regulating Protein Balance in Skeletal Muscle During Recovery From Sepsis.
Article in Shock (Augusta, Ga.), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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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
22 citing papers in PubMed, 34 citations in OpenAlex.
- A randomized controlled trial to determine whether beta-hydroxy-beta-methylbutyrate and/or eicosapentaenoic acid improves diaphragm and quadriceps strength in critically Ill mechanically ventilated patients.Critical care (London, England) · 2021Trial
- Impact of Very Early Physical Therapy During Septic Shock on Skeletal Muscle: A Randomized Controlled Trial.Critical care medicine · 2018Trial
- Review
- Autophagy selectively clears ER in TNF-α-induced muscle atrophy.Autophagy reports · 2026Article
- Prolonged sepsis triggers abnormal mitochondrial dynamics in the limb muscles and diaphragm.Molecular and cellular biochemistry · 2025Article
- Sepsis Induces Long-Term Muscle and Mitochondrial Dysfunction due to Autophagy Disruption Amenable by Urolithin A.Journal of cachexia, sarcopenia and muscle · 2025Article
- Muscle weakness after critical illness: unravelling biological mechanisms and clinical hurdles.Critical care (London, England) · 2025Review
- A Preclinical Model of Sepsis-Induced Myopathy with Disuse in Mice.Journal of visualized experiments : JoVE · 2024Article
- Autophagy ablation in skeletal muscles worsens sepsis-induced muscle wasting, impairs whole-body metabolism, and decreases survival.iScience · 2023Article
- Moderate exercise-induced dynamics on key sepsis-associated signaling pathways in the liver.Critical care (London, England) · 2023Article
- Starvation Protects Hepatocytes from Inflammatory Damage through Paradoxical mTORC1 Signaling.Cells · 2023Article
- Sepsis-Associated Muscle Wasting: A Comprehensive Review from Bench to Bedside.International journal of molecular sciences · 2023Review
- Chronic critical illness and post-intensive care syndrome: from pathophysiology to clinical challenges.Annals of intensive care · 2022Review
- MitoTEMPOL, a mitochondrial targeted antioxidant, prevents sepsis-induced diaphragm dysfunction.American journal of physiology. Lung cellular and molecular physiology · 2020Article
- The Surviving Sepsis Campaign: Basic/Translational Science Research Priorities.Critical care medicine · 2020Article
- The surviving sepsis campaign: basic/translational science research priorities.Intensive care medicine experimental · 2020Article
- Sepsis therapies: learning from 30 years of failure of translational research to propose new leads.EMBO molecular medicine · 2020Review
- The Role of Autophagy in Sepsis: Protection and Injury to Organs.Frontiers in physiology · 2019Review
- Temporally Distinct Regulation of Pathways Contributing to Cardiac Proteostasis During the Acute and Recovery Phases of Sepsis.Shock (Augusta, Ga.) · 2018Article
- Systemic bioinformatics analysis of skeletal muscle gene expression profiles of sepsis.Experimental and therapeutic medicine · 2018Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Muscle deconditioning is commonly observed in patients surviving sepsis. Little is known regarding the molecular mechanisms regulating muscle protein homeostasis during the recovery or convalescence phase. We adapted a sepsis-recovery mouse model that uses cecal ligation and puncture (CLP), followed 24 h later by cecal resection and antibiotic treatment, to identify putative cellular pathways regulating protein synthesis and breakdown in skeletal muscle. Ten days after CLP, body weight and food consumption did not differ between control and sepsis-recovery mice, but gastrocnemius weight was reduced. During sepsis-recovery, muscle protein synthesis was increased 2-fold and associated with enhanced mTOR kinase activity (4E-BP1 and S6K1 phosphorylation). The sepsis-induced increase in 4E-BP1 was associated with enhanced formation of the eIF4E-eIF4G active cap-dependent complex, while the increased S6K1 was associated with increased phosphorylation of downstream targets S6 and eIF4B. Proximal to mTOR, sepsis-recovery increased Akt and TSC2 phosphorylation, did not alter AMPK phosphorylation, and decreased REDD1 protein content. Despite the decreased mRNA content for the E3 ubiquitin ligases atrogin-1 and muscle RING-finger 1, proteasomal activity was increased 50%. In contrast, sepsis-recovery was associated with an apparent decrease in autophagy (e.g., increased ULK-1 phosphorylation, decreased LCB3-II, and increased p62). The mRNA content for IL-1β, IL-18, TNFα, and IL-6 in muscle was elevated in sepsis-recovery. During recovery after sepsis skeletal muscle responds with an increase in Akt-TSC2-mTOR-dependent protein synthesis and decreased autophagy, but full restoration of muscle protein content may be slowed by the continued stimulation of ubiquitin-proteasome activity.
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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.