Connexin hemichannels and early atrophic signaling in muscle during sepsis
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View abstract on PubMed
Summary
This summary is machine-generated.Connexin hemichannels (Cx HCs), specifically Cx43 and Cx45, play a key role in early sepsis-induced muscle dysfunction. Reducing these channels mitigates sepsis-related muscle damage and homeostasis disruption.
Area Of Science
- Biomedical Science
- Molecular Biology
- Physiology
Background
- Sepsis pathogenesis is complex, leading to high mortality (20-55%) and significant muscle dysfunction.
- Early identification of factors contributing to sepsis-related muscle dysfunction is critical for risk stratification and therapeutic development.
- The immune response during sepsis negatively impacts skeletal muscles, worsening prognosis.
Purpose Of The Study
- To investigate the role of connexin hemichannels (Cx HCs) in early muscle homeostasis changes during sepsis.
- To determine if Cx43 and Cx45 contribute to sepsis-induced skeletal muscle alterations.
Main Methods
- Utilized a cecal ligature and puncture (CLP) sepsis model in mice.
- Assessed IL-6 levels, weight loss, myofiber cross-sectional area, and resting membrane potential.
- Examined connexin expression in control and Cx43/Cx45-deficient mice.
Main Results
- CLP induced IL-6 elevation, sarcolemma permeabilization, reduced membrane potential, and ubiquitin-proteasome pathway activation in control mice.
- Mice deficient in Cx43/Cx45 exhibited significantly reduced CLP-induced muscle alterations.
- Cx43 and Cx45 expression levels were altered following CLP.
Conclusions
- Connexin hemichannels, particularly Cx43 and Cx45, are implicated in the early development of muscle alterations during sepsis.
- Targeting Cx43 and Cx45 may offer a therapeutic strategy to mitigate sepsis-related muscle dysfunction.
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