Hydrogen Sulfide—Clues from Evolution and Implication for Neonatal Respiratory Diseases

Reactive oxygen species (ROS) have been the focus of redox research in the realm of oxidative neonatal respiratory diseases such as bronchopulmonary dysplasia (BPD). Over the years, nitric oxide (NO) and carbon monoxide (CO) have been identified as important gaseous signaling molecules involved in m...

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Main Authors: Abhrajit Ganguly, Gaston Ofman, Peter F Vitiello
Format: Article
Language:English
Published: MDPI AG 2021-03-01
Series:Children
Subjects:
Online Access:https://www.mdpi.com/2227-9067/8/3/213
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author Abhrajit Ganguly
Gaston Ofman
Peter F Vitiello
author_facet Abhrajit Ganguly
Gaston Ofman
Peter F Vitiello
author_sort Abhrajit Ganguly
collection DOAJ
description Reactive oxygen species (ROS) have been the focus of redox research in the realm of oxidative neonatal respiratory diseases such as bronchopulmonary dysplasia (BPD). Over the years, nitric oxide (NO) and carbon monoxide (CO) have been identified as important gaseous signaling molecules involved in modulating the redox homeostasis in the developing lung. While animal data targeting aspects of these redox pathways have been promising in treating and/or preventing experimental models of neonatal lung disease, none are particularly effective in human neonatal clinical trials. In recent years, hydrogen sulfide (H<sub>2</sub>S) has emerged as a novel gasotransmitter involved in a magnitude of cellular signaling pathways and functions. The importance of H<sub>2</sub>S signaling may lie in the fact that early life-forms evolved in a nearly anoxic, sulfur-rich environment and were dependent on H<sub>2</sub>S for energy. Recent studies have demonstrated an important role of H<sub>2</sub>S and its synthesizing enzymes in lung development, which normally takes place in a relatively hypoxic intrauterine environment. In this review, we look at clues from evolution and explore the important role that the H<sub>2</sub>S signaling pathway may play in oxidative neonatal respiratory diseases and discuss future opportunities to explore this phenomenon in the context of neonatal chronic lung disease.
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spelling doaj.art-420ae78f13aa4eb1ba3ef25604d5740c2023-11-21T10:00:18ZengMDPI AGChildren2227-90672021-03-018321310.3390/children8030213Hydrogen Sulfide—Clues from Evolution and Implication for Neonatal Respiratory DiseasesAbhrajit Ganguly0Gaston Ofman1Peter F Vitiello2Center for Pregnancy and Newborn Research, Department of Pediatrics, Section of Neonatal-Perinatal Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104, USACenter for Pregnancy and Newborn Research, Department of Pediatrics, Section of Neonatal-Perinatal Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104, USACenter for Pregnancy and Newborn Research, Department of Pediatrics, Section of Neonatal-Perinatal Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104, USAReactive oxygen species (ROS) have been the focus of redox research in the realm of oxidative neonatal respiratory diseases such as bronchopulmonary dysplasia (BPD). Over the years, nitric oxide (NO) and carbon monoxide (CO) have been identified as important gaseous signaling molecules involved in modulating the redox homeostasis in the developing lung. While animal data targeting aspects of these redox pathways have been promising in treating and/or preventing experimental models of neonatal lung disease, none are particularly effective in human neonatal clinical trials. In recent years, hydrogen sulfide (H<sub>2</sub>S) has emerged as a novel gasotransmitter involved in a magnitude of cellular signaling pathways and functions. The importance of H<sub>2</sub>S signaling may lie in the fact that early life-forms evolved in a nearly anoxic, sulfur-rich environment and were dependent on H<sub>2</sub>S for energy. Recent studies have demonstrated an important role of H<sub>2</sub>S and its synthesizing enzymes in lung development, which normally takes place in a relatively hypoxic intrauterine environment. In this review, we look at clues from evolution and explore the important role that the H<sub>2</sub>S signaling pathway may play in oxidative neonatal respiratory diseases and discuss future opportunities to explore this phenomenon in the context of neonatal chronic lung disease.https://www.mdpi.com/2227-9067/8/3/213hydrogen sulfidebronchopulmonary dysplasiaprematurityneonatal lung diseases
spellingShingle Abhrajit Ganguly
Gaston Ofman
Peter F Vitiello
Hydrogen Sulfide—Clues from Evolution and Implication for Neonatal Respiratory Diseases
Children
hydrogen sulfide
bronchopulmonary dysplasia
prematurity
neonatal lung diseases
title Hydrogen Sulfide—Clues from Evolution and Implication for Neonatal Respiratory Diseases
title_full Hydrogen Sulfide—Clues from Evolution and Implication for Neonatal Respiratory Diseases
title_fullStr Hydrogen Sulfide—Clues from Evolution and Implication for Neonatal Respiratory Diseases
title_full_unstemmed Hydrogen Sulfide—Clues from Evolution and Implication for Neonatal Respiratory Diseases
title_short Hydrogen Sulfide—Clues from Evolution and Implication for Neonatal Respiratory Diseases
title_sort hydrogen sulfide clues from evolution and implication for neonatal respiratory diseases
topic hydrogen sulfide
bronchopulmonary dysplasia
prematurity
neonatal lung diseases
url https://www.mdpi.com/2227-9067/8/3/213
work_keys_str_mv AT abhrajitganguly hydrogensulfidecluesfromevolutionandimplicationforneonatalrespiratorydiseases
AT gastonofman hydrogensulfidecluesfromevolutionandimplicationforneonatalrespiratorydiseases
AT peterfvitiello hydrogensulfidecluesfromevolutionandimplicationforneonatalrespiratorydiseases