Reactive oxygen species-induced reactive oxygen species release in vascular signaling and disease

Young Mee Kim, Masuko Ushio-Fukai

Research output: Chapter in Book/Report/Conference proceedingChapter

Abstract

Reactive oxygen species (ROS) derived from both nicotinamide adenine dinucleotide phosphate oxidase (NOX) and mitochondria play a critical role in many physiological and pathological processes. However, how highly diffusible ROS produced from different sources can coordinate to drive angiogenesis and other responses is poorly understood. Recently, the cross-talk between NOX and mitochondria, termed “ROS-induced ROS release (RIRR)" has been proposed as a mechanism for ROS amplification and localized ROS production. NOX-derived ROS increase mitochondrial ROS while mitochondrial ROS stimulate NOX activation. This RIRR mechanism may represent a feed-forward vicious cycle of ROS production, which can be targeted under conditions of oxidative stress or enhanced in physiological condition. In this chapter, we will summarize the recent knowledge regarding the RIRR involved in vascular signaling and disease especially focusing on angiogenesis.

Original languageEnglish (US)
Title of host publicationEndothelial Signaling in Vascular Dysfunction and Disease
Subtitle of host publicationFrom Bench to Bedside
PublisherElsevier
Pages17-27
Number of pages11
ISBN (Electronic)9780128161968
DOIs
StatePublished - Jan 1 2021

Keywords

  • Angiogenesis
  • Endothelial cell
  • Reactive oxygen species
  • Redox signaling
  • Vascular endothelial growth factor

ASJC Scopus subject areas

  • General Agricultural and Biological Sciences
  • General Biochemistry, Genetics and Molecular Biology

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