ORIGINAL RESEARCH article
Front. Endocrinol.
Sec. Obesity
Volume 16 - 2025 | doi: 10.3389/fendo.2025.1630979
Pdgfrα deficiency in islet b-cells up-regulates apoptosis of b-cells and disturbs glucose metabolism in B6 mice
Provisionally accepted
LUYAO ZHANG1
Yanpeng Xing1Pai Wang1
Jianlei Gu2Jian Peng2
Juan Huang2
James Alexander Pearson3
Youjia Hu2
Hongyu Zhao2
F. Susan Wong3
Li Wen2*- 1the first hospital of Jilin University, Changchun, China
- 2School of Medicine, Yale University, New Haven, United States
- 3Cardiff University, Cardiff, United Kingdom
Select one of your emails
You have multiple emails registered with Frontiers:
Notify me on publication
Please enter your email address:
If you already have an account, please login
You don't have a Frontiers account ? You can register here
Our study offers novel insights into the role of Pdgfra in β-cell fitness and glucose metabolism in the context of obesity and/or type 2 diabetes. It further highlights the potential of PDGFRα as a modulator of metabolic processes. Therefore, targeting PDGFRα or the newly identified β-cell apoptotic factors may present opportunities for the development of novel preventive and/or therapeutic strategies for diabetes and related metabolic disorders. We believe this manuscript will be of significant interest to your readership, particularly given the growing focus on obesity and type 2 diabetes. We confirm that this work has not been presented, in whole or in part, at any external conference. There are no restrictions on data availability. All data supporting this study will be made accessible, and the sequencing data have already been deposited in the NCBI database. The authors declare no conflict of interest. We greatly appreciate your and the reviewers' time and patience, and we hope our revised manuscript meets your expectations and will be favorably considered for publication in Frontiers in Endocrinology.
Keywords: obesity,, pancreatic beta cells, PDGFR alpha, Apoptosis, ATF5, GADD45B
Received: 19 May 2025; Accepted: 03 Oct 2025.
Copyright: © 2025 ZHANG, Xing, Wang, Gu, Peng, Huang, Pearson, Hu, Zhao, Wong and Wen. 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: Li Wen, li.wen@yale.edu
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.