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The mechanism of the NFAT transcription factor family involved in oxidative stress response.

Abstract
As a transcriptional activator widely expressed in various tissues, nuclear factor of activated T cells (NFAT) is involved in the regulation of the immune system, the development of the heart and brain systems, and classically mediating pathological processes such as cardiac hypertrophy. Oxidative stress is an imbalance of intracellular redox status, characterized by excessive generation of reactive oxygen species, accompanied by mitochondrial dysfunction, calcium overload, and subsequent lipid peroxidation, inflammation, and apoptosis. Oxidative stress occurs during various pathological processes, such as chronic hypoxia, vascular smooth muscle cell phenotype switching, ischemia-reperfusion, and cardiac remodeling. Calcium overload leads to an increase in intracellular calcium concentration, while NFAT can be activated through calcium-calcineurin, which is also the main regulatory mode of NFAT factors. This review focuses on the effects of NFAT transcription factors on reactive oxygen species production, calcium overload, mitochondrial dysfunction, redox reactions, lipid peroxidation, inflammation, and apoptosis in response to oxidative stress. We hope to provide a reference for the functions and characteristics of NFAT involved in various stages of oxidative stress as well as related potential targets.
AuthorsPeiyue Zhang, Cuiyuan Huang, Haiyin Liu, Mengting Zhang, Li Liu, Yuhong Zhai, Jing Zhang, Jian Yang, Jun Yang
JournalJournal of cardiology (J Cardiol) Vol. 83 Issue 1 Pg. 30-36 (01 2024) ISSN: 1876-4738 [Electronic] Netherlands
PMID37149283 (Publication Type: Journal Article, Review, Research Support, Non-U.S. Gov't)
CopyrightCopyright © 2023. Published by Elsevier Ltd.
Chemical References
  • Reactive Oxygen Species
  • Calcium
  • NFATC Transcription Factors
Topics
  • Humans
  • Reactive Oxygen Species (pharmacology)
  • Calcium (metabolism, pharmacology)
  • Oxidative Stress
  • NFATC Transcription Factors (metabolism, pharmacology)
  • Oxidation-Reduction
  • Inflammation

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