©The Author(s) 2025. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Dec 28, 2025; 31(48): 113840
Published online Dec 28, 2025. doi: 10.3748/wjg.v31.i48.113840
Published online Dec 28, 2025. doi: 10.3748/wjg.v31.i48.113840
Mitochondrial dysfunction as a bridge to pathology in acute pancreatitis: From molecular insights to novel therapeutic strategies
Chuan-Chao Xia, Yue Xu, Guo-Qiang Xu, Department of Gastroenterology, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310003, Zhejiang Province, China
Zhen-Huan Wang, Department of Radiology, The Second Affiliated Hospital of Naval Medical University, Shanghai 200003, China
Co-first authors: Chuan-Chao Xia and Yue Xu.
Co-corresponding authors: Zhen-Huan Wang and Guo-Qiang Xu.
Author contributions: Xia CC and Xu Y wrote the manuscript as co-first authors; Wang ZH contributed to searching the literature; Xia CC and Wang ZH revised the manuscript; Xu GQ reviewed and supervised the project; Xu GQ and Wang ZH made equal contributions as co-corresponding authors. All authors have read and approved the final manuscript.
Supported by National Natural Science Foundation of China, No. 8217030254.
Conflict-of-interest statement: All the authors report no relevant conflicts of interest for this article.
Corresponding author: Guo-Qiang Xu, MD, Professor, Department of Gastroenterology, The First Affiliated Hospital, Zhejiang University School of Medicine, No. 79 Qingchun Road, Hangzhou 310003, Zhejiang Province, China. 1193065@zju.edu.cn
Received: September 5, 2025
Revised: October 28, 2025
Accepted: November 14, 2025
Published online: December 28, 2025
Processing time: 113 Days and 20.2 Hours
Revised: October 28, 2025
Accepted: November 14, 2025
Published online: December 28, 2025
Processing time: 113 Days and 20.2 Hours
Core Tip
Core Tip: Mitochondrial dysfunction is increasingly recognized as a pivotal initiating factor in acute pancreatitis (AP), preceding trypsin activation and inflammatory amplification. Key mechanisms include calcium overload, oxidative stress, mitochondrial permeability transition pore opening, and impaired mitophagy. This review synthesizes current evidence on mitochondrial dysregulation in AP and highlights emerging therapeutic strategies targeting mitochondrial pathways, offering new avenues for transitioning from supportive care to mechanism-driven precision medicine in AP management.