Zhang P, Liu SM. Letter to the Editor: Mechanistic insights into tumor necrosis factor-α-mediated islet β-cell apoptosis in acute pancreatitis-associated abnormal glucose metabolism. World J Gastroenterol 2026; 32(31): 116501 [DOI: 10.3748/wjg.116501]
Corresponding Author of This Article
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
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Immunology
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letter
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Zhang P, Liu SM. Letter to the Editor: Mechanistic insights into tumor necrosis factor-α-mediated islet β-cell apoptosis in acute pancreatitis-associated abnormal glucose metabolism. World J Gastroenterol 2026; 32(31): 116501 [DOI: 10.3748/wjg.116501]
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
Peng Zhang, Shang-Ming Liu
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
Abstract
The study by Chen et al, published in the recent issue of the World Journal of Gastroenterology, which systematically elucidate the role of tumor necrosis factor-α (TNF-α) in abnormal glucose metabolism following acute pancreatitis, demonstrating that TNF-α induces islet β-cell apoptosis through activation of the Bax/Bcl-2/caspase-3 pathway. While these findings provide mechanistic insights, the study’s scope remains limited by insufficient investigation into upstream/downstream TNF-α signaling, including the role of TNF receptor subtypes and potential crosstalk with other inflammatory or metabolic pathways. The translational potential of TNF-α inhibition in preventing pancreatitis-associated diabetes is promising, yet clinical application requires careful assessment of potential risks, including increased susceptibility to infection and impaired tissue repair, particularly during the acute inflammatory phase. Further validation in broader populations and longer-term studies is needed to establish safety, efficacy, and optimal timing for such interventions.
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.
