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REVIEW article

Front. Cell Dev. Biol.
Sec. Cell Death and Survival
Volume 12 - 2024 | doi: 10.3389/fcell.2024.1458716

CHAC1: a Master Regulator of Oxidative Stress and Ferroptosis in Human Diseases and Cancers

Provisionally accepted
Jiasen Sun Jiasen Sun Hui Ren Hui Ren Jiawen Wang Jiawen Wang Xiang Xiao Xiang Xiao Lin Zhu Lin Zhu Yanyan Wang Yanyan Wang Lili Yang Lili Yang *
  • Ankang Central Hospital, Ankang, China

The final, formatted version of the article will be published soon.

    CHAC1, an essential regulator of oxidative stress and ferroptosis, is increasingly recognized for its significant roles in these cellular processes and its impact on various human diseases and cancers. This review aims to provide a comprehensive overview of CHAC1's molecular functions, regulatory mechanisms, and effects in different pathological contexts. Specifically, the study objectives are to elucidate the biochemical pathways involving CHAC1, explore its regulatory network, and discuss its implications in disease progression and potential therapeutic strategies. As a γ-glutamyl cyclotransferase, CHAC1 degrades glutathione, affecting calcium signaling and mitochondrial function. Its regulation involves transcription factors like ATF4 and ATF3, which control CHAC1 mRNA expression. CHAC1 is crucial for maintaining redox balance and regulating cell death pathways in cancer. Its elevated levels are associated with poor prognosis in many cancers, indicating its potential as a biomarker and therapeutic target. Additionally, CHAC1 influences non-cancerous diseases such as neurodegenerative and cardiovascular disorders. Therapeutically, targeting CHAC1 could increase cancer cell sensitivity to ferroptosis, aiding in overcoming resistance to standard treatments. This review compiles current knowledge and recent discoveries, emphasizing CHAC1's vital role in human diseases and its potential in diagnostic and therapeutic applications.

    Keywords: ferroptosis, Cell Death, unfold protein response, Endoplasmic Reticulum Stress, Cancer, Glutathione

    Received: 02 Jul 2024; Accepted: 10 Sep 2024.

    Copyright: © 2024 Sun, Ren, Wang, Xiao, Zhu, Wang and Yang. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

    * Correspondence: Lili Yang, Ankang Central Hospital, Ankang, China

    Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.