Publication Name	World Journal of Gastroenterology
Manuscript ID	117268
Country	Italy

Category	Research & Experimental Medicine
Manuscript Type	Letter to the Editor
Article Title	Tumor necrosis factor-α signaling and β-cell apoptosis in acute pancreatitis: Integrating molecular mechanisms and metabolic implications
Manuscript Source	Invited Manuscript
All Author List	Lara Lizzi and Mara Massimi
Funding Agency and Grant Number
Corresponding Author	Mara Massimi, Associate Professor, PhD, Department of Life, Health and Environmental Sciences, University of L'Aquila, Via Vetoio, L'Aquila 67100, AQ, Italy. mara.massimi@univaq.it
Key Words	Tumor necrosis factor-α; β-cell apoptosis; Oxidative stress; Endoplasmic reticulum stress; Glucose metabolism; Acute pancreatitis; Post-pancreatitis diabetes mellitus; Inflammatory signaling
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.
Citation	Lizzi L, Massimi M. Tumor necrosis factor-α signaling and β-cell apoptosis in acute pancreatitis: Integrating molecular mechanisms and metabolic implications. World J Gastroenterol 2026; In press

Received	2025-12-03 00:57
Peer-Review Started	2025-12-03 00:57
First Decision by Editorial Office Director	2025-12-16 10:05
Return for Revision	2025-12-16 10:05
Revised	2025-12-23 20:09
Publication Fee Transferred
Second Decision by Editor	2026-02-10 02:43
Second Decision by Editor-in-Chief
Final Decision by Editorial Office Director	2026-02-10 11:53
Articles in Press	2026-02-10 11:53
Edit the Manuscript by Language Editor
Typeset the Manuscript

ISSN	1007-9327 (print) and 2219-2840 (online)
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