REVIEW article
Front. Pharmacol.
Sec. Cardiovascular and Smooth Muscle Pharmacology
Endoplasmic Reticulum Oxidoreductin 1α as a Potential Therapeutic Target in Diseases: From Oxidative Protein Folding to Pathophysiological Mechanisms
Provisionally accepted
- 1Affiliated Nanhua Hospital, Hengyang Medical School, University of South China, hengyang, China
- 2The Academy of Chinese Health Risks of West China Hospital, Chengdu 610041, China, chengdu, China
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Endoplasmic Reticulum Oxidoreductin 1α (ERO1α), an ER-resident thiol oxidoreductase, has been implicated in disulfide bond formation during protein folding by acting as an electron acceptor transfer for protein disulfide isomerase (PDI). This process reduces oxygen to H2O2 contributing up to 25% of the induced cellular reactive oxygen (ROS). However, research has shown that disulfide bond formation in certain proteins is preferentially catalyzed directly by ERO1, rather than indirectly through PDI. ERO1α also contributes to calcium homeostasis and endoplasmic reticulum stress (ERS). Disruption of these processes is closely associated with a variety of diseases, while the detailed molecular and cellular mechanisms underlying these processes remain to be elucidated. In mammals, tissue-specific ERO1α knockout and inhibitors have been developed to elucidate the cell-specific functions, but ERO1α inhibitors are not specific and may have significant cytotoxicity. This reviews provide an in depth summary regarding ERO1α in various disease processes, including cardiovascular diseases, diabetes, and cancer. Furthermore, it highlights the potential of ERO1α as a potential biomarker and a novel therapeutic target in clinical diseases.
Keywords: endoplasmic reticulum oxidoreductase 1α, Cardiovascular Diseases, Cancer, diabetes, Neurodegenerative Diseases
Received: 19 Sep 2025; Accepted: 03 Nov 2025.
Copyright: © 2025 fang, Xiaoyue and xiaohui. 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:
he fang, 2023030346@usc.edu.cn
Liu xiaohui, 2023030303@usc.edu.cn
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