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EDITORIAL article

Front. Physiol.
Sec. Respiratory Physiology and Pathophysiology
Volume 15 - 2024 | doi: 10.3389/fphys.2024.1508729
This article is part of the Research Topic Molecular Mechanisms of Lung Endothelial Permeability, Vol II View all 5 articles

Editorial: Molecular Mechanisms of Lung Endothelial Permeability

Provisionally accepted
Alexander Verin Alexander Verin 1,2*Rahul S. Patil Rahul S. Patil 2Narasimham L. Parinandi Narasimham L. Parinandi 3,4Evgenia Gerasimovskaya Evgenia Gerasimovskaya 5
  • 1 Medical College of Georgia, Augusta University, Augusta, United States
  • 2 Vascular Biology Center, Augusta University, Augusta, Georgia, United States
  • 3 Division of Pulmonary, Critical Care and Sleep Medicine, Department of Internal Medicine, College of Medicine, The Ohio State University, Columbus, Ohio, United States
  • 4 Wexner Medical Center, The Ohio State University, Columbus, Ohio, United States
  • 5 Department of Pediatrics, School of Medicine, University of Colorado Anschutz Medical Campus, Aurora, Colorado, United States

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

    The interplay of extracellular vehicles (EVs), endothelial cell responses, and signaling pathways presents a complex picture of the mechanisms underlying acute lung injury (ALI) and acute respiratory distress syndrome (ARDS). These severe respiratory conditions, complicated by intricate pathogenesis, highlight the role of EVs in mediating intercellular communication and represent potential for novel therapeutic approaches. In their study for the current Research Topic, Karpurapu et al. reported that EVs are crucial in transporting biologically active macromolecules between cells, particularly in the lungs. In mouse models, the activation of nuclear factor of activated T cell cytoplasmic member 3 (NFATc3) in pulmonary macrophages in response to lipopolysaccharide (LPS) has been observed. The inhibition of this activation by a novel cellpermeable calcineurin peptide inhibitor, CNI103, effectively mitigates the symptoms of ALI. EVs from the bronchoalveolar lavage fluid of LPS-treated mice contain elevated levels of arachidonic acid metabolites, directly implicating pro-inflammatory lipid mediators in lung inflammation and injury. This discovery points to a regulatory mechanism where the calcineurin-NFATc3 pathway influences the lipid content of EVs, impacting the pathogenesis of ALI. The purinergic signaling system is emerging as a critical regulatory circuit, essential for maintaining homeostatic balance and modulating pathological vascular responses in various cardiovascular and lung diseases. Despite its recognized significance, investigations into purinergic regulation specifically within the lung endothelium and vasa vasorum endothelium

    Keywords: Endothelial cells (ECs), acute lung injury (ALI), Acute respiratory distress syndrome (ARDS), nuclear factor of activated T cell cytoplasmic member 3 (NFATc3), purinergic signaling, Heat shock proteins (HSP)

    Received: 09 Oct 2024; Accepted: 11 Oct 2024.

    Copyright: © 2024 Verin, Patil, Parinandi and Gerasimovskaya. 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: Alexander Verin, Medical College of Georgia, Augusta University, Augusta, United States

    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.