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BRIEF RESEARCH REPORT article

Front. Physiol.
Sec. Membrane Physiology and Membrane Biophysics
Volume 16 - 2025 | doi: 10.3389/fphys.2025.1514769
This article is part of the Research Topic Molecular Mechanism of Ion Channel Activation and Modulation View all 5 articles

Connexin Hemichannels and Early Atrophic Signaling in Muscle during Sepsis

Provisionally accepted
Elisa Balboa Elisa Balboa 1*Fujiko Saavedra Fujiko Saavedra 2Luis Andrés Cea Luis Andrés Cea 3Aníbal A Vargas Aníbal A Vargas 4Tomas Regueira Tomas Regueira 5Juan Saez Juan Saez 6*
  • 1 Center for Biomedical Research, Finis Terrae University, Santiago, Chile
  • 2 Program of Reproductive Biology, Research and Innovation Center, School of Medicine, Faculty of Medicine, Universidad de los Andes, Santiago, Chile
  • 3 Instituto de Ciencias Biomédicas, Facultad de Ciencias de la Salud, Universidad Autónoma de Chile, Santiago, Chile
  • 4 Center for Integrative Biology, Faculty of Sciences, Major University, Santiago, Santiago Metropolitan Region (RM), Chile
  • 5 Intensive Care Department, Clínica Santa María, Santiago, Chile
  • 6 Centro Interdisciplinario de Neurociencias de Valparaíso, Universidad de Valparaíso, Valparaiso, Chile

The final, formatted version of the article will be published soon.

    Sepsis pathogenesis is complex, and effective treatments are limited, leading to high mortality rates between 20% and 55%. Early identification of factors contributing to sepsis-related muscle dysfunction is critical for risk stratification and potential therapeutic development. The immune response during sepsis affects skeletal muscles, contributing to organ dysfunction and worsening prognosis. In this study, we explore the role of connexin hemichannels (Cx HCs) in the early changes in muscle homeostasis during sepsis. Using a cecal ligature and puncture (CLP)induced sepsis model, we assessed IL-6 levels, weight loss, myofiber cross-sectional area, resting membrane potential, and connexin expression in control and Cx43/Cx45-deficient mice. CLP induced IL-6 elevation, sarcolemma permeabilization, reduced membrane potential, and activation of the ubiquitin-proteasome pathway in control mice, while Cx43/45-deficient mice exhibited reduced all CLP-induced muscle alterations. These findings suggest that Cx43 and Cx45 are involved in the early development of muscle alterations during sepsis.

    Keywords: resting membrane potential, Muscles, Inflammation, channeloapthy, connexin

    Received: 21 Oct 2024; Accepted: 24 Jan 2025.

    Copyright: © 2025 Balboa, Saavedra, Cea, Vargas, Regueira and Saez. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

    * Correspondence:
    Elisa Balboa, Center for Biomedical Research, Finis Terrae University, Santiago, Chile
    Juan Saez, Centro Interdisciplinario de Neurociencias de Valparaíso, Universidad de Valparaíso, Valparaiso, Chile

    Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.