Reactive Oxygen Species Signaling in Animal Models of Pulmonary Hypertension

Stephen Wedgwood, Satyan Lakshminrusimha, Robin H Steinhorn

Research output: Chapter in Book/Report/Conference proceedingChapter

Abstract

Pulmonary hypertension (PH) is often due to an increase in pulmonary vascular resistance (PVR) typically associated with muscularization and fibrosis of the pulmonary arterioles, decreased pulmonary blood flow and right ventricular hypertrophy (RVH). Abnormal signaling pathways triggered by elevated reactive oxygen species (ROS) during the perinatal and postnatal periods play a substantive role in the development of PH in several animal models. ROS levels become elevated when ROS-generating enzyme systems are activated and/or when ROS scavengers are inactivated. General antioxidant therapy has been largely unsuccessful, perhaps because low-level ROS signaling is essential for normal cell function. Identifying specific components of pathways triggered by ROS to induce a specific disease may reveal more attractive targets for therapy. This chapter will discuss the mechanisms by which ROS are elevated, the subsequent target molecules, and the consequences of abnormal signaling in several models of pulmonary hypertension.

Original languageEnglish (US)
Title of host publicationHypoxic Respiratory Failure in the Newborn
Subtitle of host publicationFrom Origins to Clinical Management
PublisherCRC Press
Pages101-105
Number of pages5
ISBN (Electronic)9781000442328
ISBN (Print)9780367493998
DOIs
StatePublished - Jan 1 2021

ASJC Scopus subject areas

  • Medicine(all)

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