ArticleMolecular and cellular biochemistry2025
Prolonged sepsis triggers abnormal mitochondrial dynamics in the limb muscles and diaphragm.
Article in Molecular and cellular biochemistry, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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
3 citing papers in PubMed.
- Acute mitochondrial dysfunction impairs neuromuscular transmission and contractility in mouse diaphragm: the protective potential of 25-hydroxycholesterol.Journal of physiology and biochemistry · 2026Article
- Sarcopenia and sepsis fuel a self-perpetuating cycle of immunometabolism decline.Frontiers in immunology · 2026Review
- Modulation of mitochondrial quality control in sepsis by traditional Chinese medicine: mechanistic insights and translational perspectives.Frontiers in pharmacology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
Abstract
Mitochondrial dysfunction is considered as a major trigger of sepsis-induced intensive care unit-acquired weakness (ICU-AW), but the precise role of impaired mitochondrial dynamics in sepsis-induced ICU-AW remains unclear. The cecal ligation and puncture (CLP) model was used to induce sepsis in mice. Fluid resuscitation and antibiotic treatment were used to establish a 5-day duration sepsis model, with sham-operated animals serving as controls. The muscle function of the diaphragm (DM) and tibialis anterior (TA) was assessed individually. Transmission electron microscopy (TEM) was used to observe changes in mitochondrial ultrastructure and measure the morphological parameters. Western blot analysis and quantitative real-time polymerase chain reaction were used to examine the expression of mitochondrial fusion and fission proteins and genes in DM and TA muscles. Additionally, inflammation and apoptosis were assessed in these muscles by measuring the level of pro-inflammatory cytokines and apoptotic DNA degradation, respectively. Mice subjected to CLP developed severe sepsis. Limb muscle dysfunction was more severe than that of the DM, as indicated by a greater reductions in compound muscle action potential, strength, fatigue index, and muscle fiber cross-sectional area. TEM analysis revealed sepsis-induced intermyofibrillar mitochondrial fragmentation and accumulation of injury. Both muscles showed reduced levels of Opa1 and Mfn2 mRNA and protein, and increased levels of Fis1 mRNA and protein. Correlation analysis revealed significant associations between muscle strength and Opa1, Mfn2, and Opa1/Drp1 at 5 days post-sepsis. Surviving mice at 5 days showed persistent inflammation, injury, and apoptosis in both muscles, but were more pronounced in the TA muscle. Prolonged sepsis leads to an impairment in mitochondrial dynamics, resulting in skeletal muscle weakness and atrophy, which may be one of the possible mechanisms of sepsis-induced ICU-AW.
Indexed as
Identifiers
40591175What 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.