Xia CC, Xu Y, Wang ZH, Xu GQ. Mitochondrial dysfunction as a bridge to pathology in acute pancreatitis: From molecular insights to novel therapeutic strategies. World J Gastroenterol 2025; 31(48): 113840 [DOI: 10.3748/wjg.v31.i48.113840]
Corresponding Author of This Article
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
Research Domain of This Article
Gastroenterology & Hepatology
Article-Type of This Article
Review
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This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Dec 28, 2025 (publication date) through Dec 27, 2025
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Journal Information of This Article
Publication Name
World Journal of Gastroenterology
ISSN
1007-9327
Publisher of This Article
Baishideng Publishing Group Inc, 7041 Koll Center Parkway, Suite 160, Pleasanton, CA 94566, USA
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Xia CC, Xu Y, Wang ZH, Xu GQ. Mitochondrial dysfunction as a bridge to pathology in acute pancreatitis: From molecular insights to novel therapeutic strategies. World J Gastroenterol 2025; 31(48): 113840 [DOI: 10.3748/wjg.v31.i48.113840]
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.
Open Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/
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 18.8 Hours
Abstract
Acute pancreatitis (AP) is a life-threatening inflammatory condition triggered by the premature activation of trypsin. The limited understanding of its underlying pathophysiology remains a key obstacle to the development of targeted therapies. Mounting evidence now underscores mitochondrial dysfunction as a critical pathogenic driver in AP. Cellular mitochondrial dysfunction often precedes both cytokine release and trypsin activation, potentially serving as a primary initiator in the development and advancement of AP. Mitochondrial dysfunction is associated with calcium overload, inflammatory reactions, mitochondrial permeability transition pore opening, mitophagy damage, and other potential pathogenesis of pancreatic cell injury. Elucidating the impact of mitochondrial injury in AP may facilitate the development of innovative treatment approaches. This review provides a comprehensive and systematic analysis of the pivotal role of mitochondria in regulating pancreatic homeostasis, while evaluating emerging therapeutic strategies aimed at mitigating mitochondrial dysfunction. By integrating cutting-edge research findings, this work highlights the translational potential of these advancements in redefining diagnostic frameworks and optimizing therapeutic approaches for the management of AP.
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.
