Reprint

Roles and Functions of ROS and RNS in Cellular Physiology and Pathology

Edited by
April 2020
230 pages
  • ISBN978-3-03928-782-6 (Hardback)
  • ISBN978-3-03928-783-3 (PDF)

This book is a reprint of the Special Issue Roles and Functions of ROS and RNS in Cellular Physiology and Pathology that was published in

Biology & Life Sciences
Medicine & Pharmacology
Summary
Our common knowledge on oxidative stress has evolved substantially over the years and has been mostly focused on the fundamental chemical reactions and the most relevant chemical species involved in the human pathophysiology of oxidative stress-associated diseases. Thus, reactive oxygen species and reactive nitrogen species (ROS and RNS) were identified as the key players initiating, mediating, and regulating the cellular and biochemical complexity of oxidative stress either as physiological (acting pro-hormetic) or as pathogenic (causing destructive vicious circle) process. The papers published in this particular Special Issue of the Cells demonstrate the impressive pathophysiological relevance of ROS and RNS in a range of contexts, including the relevance of second messengers of free radicals like 4-hydroxynonenal, allowing us to assume that even more detailed mechanisms of their positive and negative effects lie in wait, and should assist in better monitoring of the major modern diseases and the development of advanced integrative biomedicine treatments.
Format
  • Hardback
License
© 2020 by the authors; CC BY-NC-ND license
Keywords
human neuroblastoma SH-SY5Y cells; TRPM2 channel; ROS; neuronal cell death; histamine; calcium; endothelial cells; NADPH-oxidase; VAS2870; von Willebrand factor; aorta; relaxation; reactive oxygen species (ROS); oxidative stress; lipid peroxidation; acrolein; 4-hydroxynonenal (4-HNE); oxidative burst; granulocytes; cancer cells; growth control; cancer regression; hydroxyapatite-based biomaterials; osteoblast growth; redox balance; vitamins; lipid peroxidation; 4-hydroxynonenal; oxidative stress; oxidative stress; nuclear factor erythroid 2–related factor 2; heme-oxygenase-1; macrophages; plaque vulnerability; optical coherence tomography; reactive oxygen species; free radicals; DNA damage; cyclopurines; DNA and RNA polymerases; nucleotide excision repair; LC-MS/MS; xeroderma pigmentosum; cancer; intermittent hypoxia; mitochondria; Ca2+, ROS; antioxidant; free radicals; antimicrobial; toll-like receptors; cannabidiol; UV radiation; keratinocytes; antioxidants; inflammation; intracellular signaling; Nrf2; NFκB; glucose deprivation; glutamine deprivation; viability; proliferation; ROS; NRF2-NQO1 axis; IMR-90; NQO1 transcript variants; rs1800566; TP53 mutation; oxidative stress; MFN2; mitochondria; fusion/fission; oxidative stress; blood–brain barrier; bEnd5; bEnd.3; glutathione; viability; free radicals; redox balance; cell signaling; growth; toxicity; antioxidants; oxidative homeostasis; oxidative metabolism of the cells; pathophysiology of oxidative stress