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Articles Published Processes
9/4/2026 5:57:44 AM | Browse: 1 | Download: 0
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Received |
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2025-12-01 01:45 |
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Peer-Review Started |
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2025-12-01 01:45 |
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First Decision by Editorial Office Director |
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2025-12-30 07:46 |
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Return for Revision |
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2025-12-30 11:58 |
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Revised |
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2026-01-06 14:18 |
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Publication Fee Transferred |
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Second Decision by Editor |
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2026-01-20 02:36 |
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Second Decision by Editor-in-Chief |
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Final Decision by Editorial Office Director |
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2026-01-20 04:22 |
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Articles in Press |
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2026-01-20 04:22 |
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Edit the Manuscript by Language Editor |
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Typeset the Manuscript |
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2026-08-20 07:09 |
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Publish the Manuscript Online |
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2026-09-04 05:57 |
| ISSN |
1948-9358 (online) |
| 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/ |
| Copyright |
© The Author(s) 2026. Published by Baishideng Publishing Group Inc. All rights reserved. |
| Article Reprints |
For details, please visit: http://www.wjgnet.com/bpg/gerinfo/247
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| Permissions |
For details, please visit: http://www.wjgnet.com/bpg/gerinfo/207
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| Publisher |
Baishideng Publishing Group Inc, 7041 Koll Center Parkway, Suite 160, Pleasanton, CA 94566, USA |
| Website |
http://www.wjgnet.com |
| Category |
Endocrinology & Metabolism |
| Manuscript Type |
Editorial |
| Article Title |
Pancreatic injury and glucose metabolism dysfunction: The central role of inflammatory signaling and islet β-cell apoptosis
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| Manuscript Source |
Invited Manuscript |
| All Author List |
Fang-Fang Qi, Ying Zhang, Chang-Quan Liu, Hong-Jin Chen and Ai-Fang Wang |
| ORCID |
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| Funding Agency and Grant Number |
| Funding Agency |
Grant Number |
| National Natural Science Foundation of China |
No. 82260567 |
| Science and Technology Program of Guizhou Province |
No. ZK[2023]321 |
| Qiankehe Platform Project |
No. KXJZ[2024]004 |
| Taizhou Social Development Science and Technology Plan Project |
No. 23ywb146 |
| Key Laboratory of Emergency and Trauma (Hainan Medical University), Ministry of Education |
No. KLET-202502 |
| Excellent Young Talents Plan of Guizhou Medical University |
No. [2023]112 |
| Guizhou Medical University Key Laboratory of Cardiovascular Disease Basic and Clinical Research |
No. 2024001 |
| Start-Up Fund of Guizhou Medical University |
No. J2021032 |
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| Corresponding Author |
Ai-Fang Wang, MD, Department of Endocrinology, The People’s Hospital of Yuhuan (Yuhuan People’s Hospital Health Community Group), No. 18 Changle Road, Chengguan, Taizhou 317600, Zhejiang Province, China. wangaifang19832024@163.com |
| Key Words |
Acute pancreatitis; Glucose metabolism; β-cell apoptosis; Tumor necrosis factor-α; Bax/Bcl-2/caspase-3 pathway; Post-pancreatitis diabetes mellitus |
| Core Tip |
This editorial elucidates a key mechanism through which acute pancreatitis (AP) contributes to the development of diabetes: tumor necrosis factor-α (TNF-α) triggers islet β-cell apoptosis via the Bax/Bcl-2/caspase-3 pathway. We underscore the central role of this inflammatory axis in post-pancreatitis diabetes mellitus (PPDM) and advocate for targeting TNF-α as a translatable strategy to preserve β-cell mass and prevent diabetes following pancreatic injury. |
| Publish Date |
2026-09-04 05:57 |
| Citation |
Qi FF, Zhang Y, Liu CQ, Chen HJ, Wang AF. Pancreatic injury and glucose metabolism dysfunction: The central role of inflammatory signaling and islet β-cell apoptosis. World J Diabetes 2026; 17(9): 117159
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| URL |
https://www.wjgnet.com/1948-9358/full/v17/i9/117159.htm |
| DOI |
https://doi.org/10.4239/wjd.117159 |
Copyright © 1993-2026 Baishideng Publishing Group Inc, 7041 Koll Center Parkway, Suite 160, Pleasanton, CA 94566, USA. All rights reserved, including rights relating to text and data mining, AI training, and similar technologies. For open-access content, the applicable copyright and licensing terms govern.