Role of the Nrf2/HO-1 axis in bronchopulmonary dysplasia and hyperoxic lung injuries.

Abstract

Bronchopulmonary dysplasia (BPD) is a chronic illness that usually originates in preterm newborns. Generally, BPD is a consequence of respiratory distress syndrome (RDS) which, in turn, comes from the early arrest of lung development and the lack of pulmonary surfactant. The need of oxygen therapy to overcome premature newborns' compromised respiratory function generates an increasing amount of reactive oxygen species (ROS), the onset of sustained oxidative stress (OS) status, and inflammation in the pulmonary alveoli deputies to respiratory exchanges. BPD is a severe and potentially life-threatening disorder that in the most serious cases, can open the way to neurodevelopmental delay. More importantly, there is no adequate intervention to hamper or treat BPD. This perspective article seeks to review the most recent and relevant literature describing the very early stages of BPD and hyperoxic lung injuries focussing on nuclear factor erythroid derived 2 (Nrf2)/heme oxygenase-1 (HO-1) axis. Indeed, Nrf2/HO1 activation in response to OS induced lung injury in preterm concurs to the induction of certain number of antioxidant, anti-inflammatory, and detoxification pathways that seem to be more powerful than the activation of one single antioxidant gene. These elicited protective effects are able to counteract/mitigate all multifaceted aspects of the disease and may support novel approaches for the management of BPD.

• Authors: Emanuele Amata, Valeria Pittalà, Agostino Marrazzo, Carmela Parenti, Orazio Prezzavento, Emanuela Arena, Seyed Mohammad Nabavi, Loredana Salerno
• Journal: Clinical science (London, England : 1979) (Clin Sci (Lond)) Vol. 131 Issue 14 Pg. 1701-1712 (Jul 15 2017) ISSN: 1470-8736 [Electronic] England
• PMID: 28667068 (Publication Type: Journal Article, Review)
• Copyright: © 2017 The Author(s). Published by Portland Press Limited on behalf of the Biochemical Society.

Chemical References

• NF-E2-Related Factor 2
• NFE2L2 protein, human
• HMOX1 protein, human
• Heme Oxygenase-1

Topics

• Bronchopulmonary Dysplasia (physiopathology, therapy)
• Heme Oxygenase-1 (physiology)
• Humans
• Hyperoxia (physiopathology)
• Lung Injury (physiopathology)
• NF-E2-Related Factor 2 (physiology)
• Oxidative Stress (physiology)