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Antioxidants
Special Issues
Role of Redox in Pulmonary Vascular Diseases
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Role of Redox in Pulmonary Vascular Diseases

A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "Health Outcomes of Antioxidants and Oxidative Stress".

Deadline for manuscript submissions: 1 July 2025 | Viewed by 2874

Special Issue Editors

Prof. Dr. Michael S. Wolin

E-Mail Website
Guest Editor
Department of Physiology, Basic Sciences Building, New York Medical College, Valhalla, NY 10595, USA
Interests: guanylate cyclase and protein kinase G redox regulation; hypoxia; metabolic and redox signaling; oxygen sensing; pulmonary hypertension; vascular redox regulation
Prof. Dr. Sachin Gupte

E-Mail Website
Guest Editor
Department of Pharmacology, Basic Sciences Building, New York Medical College, Valhalla, NY 10595, USA
Interests: redox signalling; metabolic reprogramming; transcriptomics; epigenetic regulation; DNA and histone methylation

Special Issue Information

Dear Colleagues,

Previous studies on the physiology and pathophysiology of pulmonary circulation have provided a rich history of evidence for the multiple roles redox mechanisms play in physiological function and in contributing to pulmonary vascular disease processes in various cell types that influence lung vascular biology. Many aspects of these mechanisms remain to be defined and are potentially important in regulating hypoxia; vascular remodeling; metabolic reprogramming; transcriptomic reprogramming; roles for inflammatory mechanisms influencing pathophysiology; the cell biology of defense mechanisms in the lung; and cell-to-cell communications in the lung contributing to or protecting against pulmonary vascular disease. Thus, we welcome the submission of original research papers or review articles focused on new aspects of redox mechanisms in this field.   

Prof. Dr. Michael S. Wolin
Prof. Dr. Sachin Gupte
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Antioxidants is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • hypoxic pulmonary vasoconstriction
  • metabolic redox regulation
  • pulmonary circulation
  • pulmonary hypertension
  • pulmonary vascular disease
  • redox signaling

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Published Papers (2 papers)

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Research

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12 pages, 2220 KiB  
Article
Lung EC-SOD Overexpression Prevents Hypoxia-Induced Platelet Activation and Lung Platelet Accumulation
by Daniel Colon Hidalgo, Mariah Jordan, Janelle N. Posey, Samuel D. Burciaga, Thi-Tina N. Nguyen, Christina Sul, Caitlin V. Lewis, Cassidy Delaney and Eva S. Nozik
Antioxidants 2024, 13(8), 975; https://doi.org/10.3390/antiox13080975 - 10 Aug 2024
Cited by 3 | Viewed by 1628
Abstract
Pulmonary hypertension (PH) is a progressive disease marked by pulmonary vascular remodeling and right ventricular failure. Inflammation and oxidative stress are critical in PH pathogenesis, with early pulmonary vascular inflammation preceding vascular remodeling. Extracellular superoxide dismutase (EC-SOD), a key vascular antioxidant enzyme, mitigates [...] Read more.
Pulmonary hypertension (PH) is a progressive disease marked by pulmonary vascular remodeling and right ventricular failure. Inflammation and oxidative stress are critical in PH pathogenesis, with early pulmonary vascular inflammation preceding vascular remodeling. Extracellular superoxide dismutase (EC-SOD), a key vascular antioxidant enzyme, mitigates oxidative stress and protects against inflammation and fibrosis in diverse lung and vascular disease models. This study utilizes a murine hypobaric hypoxia model to investigate the role of lung EC-SOD on hypoxia-induced platelet activation and platelet lung accumulation, a critical factor in PH-related inflammation. We found that lung EC-SOD overexpression blocked hypoxia-induced platelet activation and platelet accumulation in the lung. Though lung EC-SOD overexpression increased lung EC-SOD content, it did not impact plasma extracellular SOD activity. However, ex vivo, exogenous extracellular SOD treatment specifically blunted convulxin-induced platelet activation but did not blunt platelet activation with thrombin or ADP. Our data identify platelets as a novel target of EC-SOD in response to hypoxia, providing a foundation to advance the understanding of dysregulated redox signaling and platelet activation in PH and other chronic hypoxic lung diseases. Full article
(This article belongs to the Special Issue Role of Redox in Pulmonary Vascular Diseases)
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Review

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41 pages, 1650 KiB  
Review
The Role of Hydrogen Sulfide in the Regulation of the Pulmonary Vasculature in Health and Disease
by Philip I. Aaronson
Antioxidants 2025, 14(3), 341; https://doi.org/10.3390/antiox14030341 - 14 Mar 2025
Viewed by 794
Abstract
The gasotransmitter hydrogen sulfide (H2S; also termed sulfide) generally acts as a vasodilator in the systemic vasculature but causes a paradoxical constriction of pulmonary arteries (PAs). In light of evidence that a fall in the partial pressure in oxygen (pO2 [...] Read more.
The gasotransmitter hydrogen sulfide (H2S; also termed sulfide) generally acts as a vasodilator in the systemic vasculature but causes a paradoxical constriction of pulmonary arteries (PAs). In light of evidence that a fall in the partial pressure in oxygen (pO2) increases cellular sulfide levels, it was proposed that a rise in sulfide in pulmonary artery smooth muscle cells (PASMCs) is responsible for hypoxic pulmonary vasoconstriction, the contraction of PAs which develops rapidly in lung regions undergoing alveolar hypoxia. In contrast, pulmonary hypertension (PH), a sustained elevation of pulmonary artery pressure (PAP) which can develop in the presence of a diverse array of pathological stimuli, including chronic hypoxia, is associated with a decrease in the expression of sulfide -producing enzymes in PASMCs and a corresponding fall in sulfide production by the lung. Evidence that PAP in animal models of PH can be lowered by administration of exogenous sulfide has led to an interest in using sulfide-donating agents for treating this condition in humans. Notably, intracellular H2S exists in equilibrium with other sulfur-containing species such as polysulfides and persulfides, and it is these reactive sulfur species which are thought to mediate most of its effects on cells through persulfidation of cysteine thiols on proteins, leading to changes in function in a manner similar to thiol oxidation by reactive oxygen species. This review sets out what is currently known about the mechanisms by which H2S and related sulfur species exert their actions on pulmonary vascular tone, both acutely and chronically, and discusses the potential of sulfide-releasing drugs as treatments for the different types of PH which arise in humans. Full article
(This article belongs to the Special Issue Role of Redox in Pulmonary Vascular Diseases)
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