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REVIEW article
Front. Physiol.
Sec. Redox Physiology
Volume 16 - 2025 | doi: 10.3389/fphys.2025.1562626
This article is part of the Research Topic Rising Stars in Redox Physiology View all articles
Endothelial ENaC as a repressor of oxidative stress and a guardian of lung capillary barrier function in bacterial and viral pneumonia
Provisionally accepted
Douglas C Eaton 1
Maritza Romero 2
Michael Anthony Matthay 3
Juerg Hamacher 4
Aarushi Advani 5 Abby Wolf 5 Trinad Chakraborty 6
Mobarak Abu Mraheil 6
Abdullah Kutlar 5
David W Stepp 7
Eric J. Belin De Chantemele 7
Felix Kraft 8
Markus Zeitlinger 8 Peter Kranke 9
Sandra Frank 10 Yunchao Su 11
Alexander A Verin 7
David JR Fulton 7
Masuko Ushio-Fukai 7
Tohru Fukai 7
Rudolf Lucas 2*- 1 Dept of Medicine,, School of Medicine, Emory University, Atlanta, Georgia, United States
- 2 Vascular Biology Center, Dept of Pharmacology and Toxicology and Division of Pulmonary Critical Care and Sleep Medicine, Medical College of Georgia at Augusta University, Augusta, United States
- 3 Cardiovascular Research Institute, Department of Pediatrics, University of California San Francisco, San Francisco, California, United States
- 4 University Hospital of Bern, Bern, Bern, Switzerland
- 5 Dept. of Medicine, Medical College of Georgia, Augusta University,, Augusta, Georgia, United States
- 6 Institute for Medical Microbiology, Faculty of Medicine, University of Giessen, Giessen, Germany
- 7 Vascular Biology Center, Augusta University, Augusta, Georgia, United States
- 8 Department of Anesthesia, Medical University of Vienna, Vienna, Austria
- 9 Dept of Anesthesiology, Critical Care, Emergency and Pain Medicine, University Hospital of Würzburg, Würzburg, Germany
- 10 Department of Anaesthesiology, LMU University Hospital, Munich, Bavaria, Germany
- 11 Department of Pharmacology and Toxicology, Medical College of Georgia, Augusta University, Augusta, Georgia, United States
The endothelium represents a crucial regulator of vascular homeostasis. Since endothelial cells mainly rely on glycolysis rather than on oxidative phosphorylation for their ATP generation, this allows capillaries to transport the maximum amount of oxygen to oxygen-starved tissues, where it can be used for energy generation. However, the occasionally high levels of oxygen and of reactive oxygen species (ROS) in the blood vessels requires a balancing act between pro-and anti-oxidative mechanisms in the endothelium. When this balance is disturbed by excessive oxidative stress, as can occur in bacterial and viral pneumonia, endothelial barrier function can be compromised. This review will discuss some of the recently discovered barrier-protective mechanisms during bacterial and viral pneumonia, mediated through the reduction of oxidative stress in lung capillaries by the epithelial sodium channel (ENaC).
Keywords: NADPH Oxidase, Epithelial Sodium Channel, Capillary endothelium, alveolarcapillary barrier function, Pneumonia, TNF, TIP peptide
Received: 17 Jan 2025; Accepted: 26 Mar 2025.
Copyright: © 2025 Eaton, Romero, Matthay, Hamacher, Advani, Wolf, Chakraborty, Abu Mraheil, Kutlar, Stepp, Belin De Chantemele, Kraft, Zeitlinger, Kranke, Frank, Su, Verin, Fulton, Ushio-Fukai, Fukai and Lucas. 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:
Rudolf Lucas, Vascular Biology Center, Dept of Pharmacology and Toxicology and Division of Pulmonary Critical Care and Sleep Medicine, Medical College of Georgia at Augusta University, Augusta, United States
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