Reprint

Molecular Targets of Oxidative Stress: Focus on the Nrf2 Signaling Pathway in Health and Disease

Edited by
October 2024
360 pages
  • ISBN978-3-7258-2227-0 (Hardback)
  • ISBN978-3-7258-2228-7 (PDF)

Print copies available soon

This is a Reprint of the Special Issue Molecular Targets of Oxidative Stress: Focus on the Nrf2 Signaling Pathway in Health and Disease that was published in

Biology & Life Sciences
Summary

Oxidative stress, known to increase the risk of multiple metabolic and chronic disorders or cancer development, is defined as an imbalance between the production of reactive oxygen species (ROS) and the capacity of antioxidants to counteract the deleterious effects of oxidants. To regulate the oxidation/reduction (redox) balance, numerous antioxidant enzymes and nonenzymatic antioxidants exist. Free radicals activate transcription factors to promote antioxidant production and mitochondrial biogenesis. One of these transcription factors, nuclear factor erythroid 2-related factor 2 (Nrf2), is a master regulator of antioxidant and anti-inflammatory responses. Indeed, Nrf2 contributes to redox balance by initiating the transcription of hundreds of genes involved in antioxidant and cytoprotective responses. A better understanding of the molecular targets of oxidative stress and their interaction with the Nrf2 signaling pathway would strengthen the relevance of their preventive or therapeutic use in health and diseases. Most of the studies presented in this Special Issue were dedicated to multiple metabolic and chronic disorders or cancer development. They contribute to improving our understanding of the molecular targets of oxidative stress and their interaction with the Nrf2 signaling pathway in some oxidative-stress-related diseases.

Format
  • Hardback
License and Copyright
© 2024 by the authors; CC BY-NC-ND license
Keywords
ASCT2; glutamate-glutamine cycle; glutaminase; glutamine synthase; glutathione synthetase; iNOS; S-nitrosylated cysteine; xCT; neurological manifestations; long-COVID; antioxidant enzymes; glutathione transferases; polymorphisms; Nrf2; spinal cord injury; phrenic motoneuron; AMPK; neuroinflammation; antioxidant; rat; NRF2; amyotrophic lateral sclerosis; C9orf72; dipeptide repeat proteins; Nrf2; obesity; lipid metabolism; chronic inflammation; oxidative stress; glucoraphanin; inflammatory bowel diseases; DSS; NRF2; oxidative stress; mitochondrial homeostasis; Nrf2; skeletal muscle; exercise; proteomics; radiation; low dose-rate; mesenchymal stem cells; human microvascular endothelial cells; RNAseq; gene regulation; Nrf2; Hsp90; ERK; JNK; Cdk5; Pin1; HO-1; phosphorylation; acetylation; ubiquitination; intracellular degradation; ligand-dependent stability; cancer; neurological disorders; oxidative stress; exosomes; miRNA; non-pigmented ciliary epithelium; trabecular meshwork; primary open-angle glaucoma; Alzheimer’s disease; antioxidant response; electrophilic activators; multitargeting compounds; Nrf2 inducers; protein–protein interaction inhibitors; oxidative stress; Parkinson’s disease; depression; Nuclear factor erythroid-2 (Nrf2); pathophysiology; antioxidant pathways; Haemoxygenase (HO-1); Nuclear factor kappa B (NF-κB); rutin; UVA-induced damage; Nrf2 pathway; oxidative stress; mitochondrial function; thyroid hormones; oxidative stress; antioxidants; Nrf2; cardioprotection; Nrf2; THP-1-derived macrophages; alveolar macrophages; repetitive magnetic stimulation; p38 MAPK; p62; Nrf2 knockout mice; Keap1; Staphylococcus aureus; NRF2; ferroptosis; antioxidant; metabolism; Ehretia tinifolia; anti-inflammatory; antioxidant; MAPK; NF-κB; Nrf2; n/a