Letter to the Editor: Tumor necrosis factor-α signaling and β-cell apoptosis in acute pancreatitis - integrating molecular mechanisms and metabolic implications

doi:10.3748/wjg.117268

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World Journal of Gastroenterology

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1007-9327

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Baishideng Publishing Group Inc, 7041 Koll Center Parkway, Suite 160, Pleasanton, CA 94566, USA

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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. Jul 21, 2026; 32(27): 117268
Published online Jul 21, 2026. doi: 10.3748/wjg.117268

Letter to the Editor: Tumor necrosis factor-α signaling and β-cell apoptosis in acute pancreatitis - integrating molecular mechanisms and metabolic implications

Lara Lizzi, Mara Massimi

Lara Lizzi, Mara Massimi, Department of Life, Health and Environmental Sciences, University of L'Aquila, L'Aquila 67100, AQ, Italy

Author contributions: Massimi M conceived the overall concept and outline, drafted the manuscript, and supervised the work; Lizzi L contributed to the development of the figure and to the discussion and literature review. Both authors critically revised the manuscript and approved the final version.

Conflict-of-interest statement: The authors declare no conflicts of interest.

Corresponding author: Mara Massimi, PhD, Associate Professor, Department of Life, Health and Environmental Sciences, University of L'Aquila, Via Vetoio, L'Aquila 67100, AQ, Italy. mara.massimi@univaq.it

Received: December 3, 2025
Revised: December 23, 2025
Accepted: February 10, 2026
Published online: July 21, 2026
Processing time: 213 Days and 13.6 Hours

Core Tip

Core Tip: Tumor necrosis factor-α (TNF-α) contributes to dysglycemia after acute pancreatitis not only by activating apoptotic pathways, but also by coordinating a broader network of inflammatory, oxidative, endoplasmic reticulum stress, and metabolic signals that impair β-cell function. Recognizing TNF-α as an upstream integrator, rather than a single apoptotic trigger, helps explain the heterogeneity of post-pancreatitis dysglycemia and highlights new therapeutic opportunities aimed at enhancing β-cell metabolic resilience.