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Copyright: ©Author(s) 2026. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution-NonCommercial (CC BY-NC 4.0) license. No commercial re-use. See permissions. Published by Baishideng Publishing Group Inc.
World J Gastroenterol. Aug 21, 2026; 32(31): 116501
Published online Aug 21, 2026. doi: 10.3748/wjg.116501
Letter to the Editor: Mechanistic insights into tumor necrosis factor-α-mediated islet β-cell apoptosis in acute pancreatitis-associated abnormal glucose metabolism
Shang-Ming Liu, Peng Zhang
Peng Zhang, Shang-Ming Liu, Medical Basic Experiment Teaching Center, School of Basic Medical Sciences, Shandong University, Jinan 250012, Shandong Province, China
Co-corresponding authors: Peng Zhang and Shang-Ming Liu.
Author contributions: Zhang P wrote the original draft; Liu SM contributed to conceptualization, writing, reviewing and editing; Zhang P and Liu SM participated in drafting the manuscript; all authors have read and approved the final version of the manuscript.
AI contribution statement: The authors used AI-based tools ChatGPT (OpenAI) during the preparation of the manuscript for language editing and formatting. After using this tool, the authors reviewed and edited the content as needed and take full responsibility for the content of the published article.
Conflict-of-interest statement: The authors declare that they have no conflict of interest.
Corresponding author: Peng Zhang, PhD, Medical Basic Experiment Teaching Center, School of Basic Medical Sciences, Shandong University, No. 44 Wenhua West Road, Lixia District, Jinan 250012, Shandong Province, China. zhangpeng1990@sdu.edu.cn
Received: November 17, 2025
Revised: January 4, 2026
Accepted: March 4, 2026
Published online: August 21, 2026
Processing time: 260 Days and 17.7 Hours
Core Tip

Core Tip: Chen et al demonstrate the role of tumor necrosis factor-α (TNF-α) in promoting islet β-cell apoptosis via the Bax/Bcl-2/caspase-3 pathway during acute pancreatitis, which contributes to abnormal glucose metabolism. While acknowledging the therapeutic potential of TNF-α inhibition, the letter highlights limitations such as unexplored upstream signaling and clinical issues, urging future research into broader mechanisms and prospective validations.

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