Basic Study
Copyright ©The Author(s) 2025. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Exp Med. Sep 20, 2025; 15(3): 103948
Published online Sep 20, 2025. doi: 10.5493/wjem.v15.i3.103948
PI3K/AKT/GSK3β regulatory axis in bone mesenchymal stem cells initiates diabetic myocardial infarction via miR-142-3p
Ning Gao, Peng-Fei Wu, Ming-Wen Wu, Yu-Meng Li, Xu Liang, Fei-Fei Wang, Xue-Jing Li, Qing-Qing Shen, Tian-Peng Zheng, Xiao-Ling Liu, Yi Sun, Liu-Xue Yang
Ning Gao, Peng-Fei Wu, Fei-Fei Wang, Xue-Jing Li, Qing-Qing Shen, Tian-Peng Zheng, Liu-Xue Yang, Department of Endocrinology, The Second Affiliated Hospital of Guiln Medical University, Guilin 541004, Guangxi Zhuang Autonomous Region, China
Ming-Wen Wu, Xu Liang, Yi Sun, Department of Toxicology, Key Laboratory of Environmental Exposommics and Entire Lifecycle Heath, Guilin Medical University, Guilin 541004, Guangxi Zhuang Autonomous Region, China
Yu-Meng Li, Occupational Disease Prevention and Control Section, Zaozhuang Center for Disease Control and Prevention, Zaozhuang 277000, Shandong Province, China
Xiao-Ling Liu, Department of Endocrinology, The First Affiliated Hospital of Guilin Medical University, Guilin 541004, Guangxi Zhuang Autonomous Region, China
Co-first authors: Ning Gao and Peng-Fei Wu.
Co-corresponding authors: Yi Sun and Liu-Xue Yang.
Author contributions: Gao N and Wu MW contributed to methodology; Li YM contributed to validation; Wang FF contributed to formal analysis; Liang X contributed to investigation; Wu PF contributed to resources; Li XJ contributed to data curation; Liu XL and Sun Y contributed to writing–original draft preparation; Shen QQ and Zheng TP contributed to writing–review and editing; Yang LX contributed to supervision, project administration, funding acquisition; All authors have read and approved the final manuscript.
Supported by Health Commission Project, No. Z2014334; and Natural Science Foundation of Guangxi Province, China, No. 2020GXNSFAA238036.
Institutional animal care and use committee statement: All procedures involving animals were reviewed and approved by the Institutional Animal Care and Use Committee of the Ethics Committee of Guilin Medical University (IACUC protocol number: GLMC-IACUC-2023009).
Conflict-of-interest statement: The author declares that they have no competitive interests.
ARRIVE guidelines statement: The authors have read the ARRIVE guidelines, and the manuscript was prepared and revised according to the ARRIVE guidelines.
Data sharing statement: sharing statement: No additional data are available.
Open Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Yi Sun, Department of Toxicology, Key Laboratory of Environmental Exposommics and Entire Lifecycle Heath, Guilin Medical University, No. 1 Zhiyuan Road, Lingui District, Guilin 541004, Guangxi Zhuang Autonomous Region, China. sunyide163@163.com
Received: December 6, 2024
Revised: March 12, 2025
Accepted: April 27, 2025
Published online: September 20, 2025
Processing time: 250 Days and 3.4 Hours
Core Tip

Core Tip: This study demonstrated that using bones mesenchymal stem cells (BMCs) as an intervention can simultaneously reduce blood sugar levels and promote hypoxic myocardial recovery. However, when miR-142-3p expression in BMCs was low, there was a reduced therapeutic efficacy of BMCs and activation of PI3K/AKT/GSK-3β. The regulatory axis regulates changes in the protein expression levels of the ferroptosis-related genes GPX4/CHCHD6. These findings suggest that miR-142-3p via the PI3K/AKT/GSK-3β regulation axis that jointly inhibits ferroptosis, may be one of the therapeutic mechanisms of BMCs in diabetic myocardial infarction.