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August 1, 2025Journal of Cachexia Sarcopenia and MuscleOpen Access

Sepsis Induces Long‐Term Muscle and Mitochondrial Dysfunction due to Autophagy Disruption Amenable by Urolithin A

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Authors

APAlexandre PierreRFRaphaël FavoryBBBenoît Brassart

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Overview

Observational analysis reveals mitochondrial dysfunction in sepsis survivors, suggesting urolithin A may enhance autophagy.

Key Points

  • Mitochondrial dysfunction after sepsis leads to significant muscle weakness, impacting physical disability in survivors.
  • Sepsis-surviving mice showed a 45% reduction in mitochondrial oxygen consumption, highlighting mitochondrial impairments.
  • Methodology included bioinformatic analysis and murine models to assess muscle and mitochondrial changes post-sepsis.
  • Urolithin A improved muscle function and mitochondrial recovery in sepsis-survivors, supporting its potential therapeutic role.

Cite This Study

Pierre et al. (2025) studied this question.

synapsesocial.com/papers/68af2b68cf1dd9ea359e4d1chttps://doi.org/10.1002/jcsm.70041
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1RAGE contributes to persistent sepsis-induced muscle and mitochondrial alterations2025
  2. 2Selenomethionine Attenuates Sepsis-Induced Skeletal Muscle Atrophy by Inhibiting ROS/NLRP3 Signaling2025 · 8 citations
  3. 3Progression of Peripheral Blood Mononuclear Cell Mitochondrial Function during the Early Phase of Sepsis in Intensive Care Unit Patients2025
  4. 4Abstract Fri139: Endotoxemia induces mitochondrial DNA (mtDNA) damage in mouse myocardium and cardiomyocytes2025
  5. 5Time-Resolved Metabolomics Reveals Mitochondrial Protection in Septic Liver Injury2025