Publication Name	World Journal of Gastroenterology
Manuscript ID	113840
Country	China

Category	Gastroenterology & Hepatology
Manuscript Type	Review
Article Title	Mitochondrial dysfunction as a bridge to pathology in acute pancreatitis: From molecular insights to novel therapeutic strategies
Manuscript Source	Unsolicited Manuscript
All Author List	Chuan-Chao Xia, Yue Xu, Zhen-Huan Wang and Guo-Qiang Xu
Funding Agency and Grant Number	Funding Agency Grant Number National Natural Science Foundation of China 8217030254
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
Key Words	Acute pancreatitis; Mitochondria; Mitochondrial dysfunction; Molecular mechanism; Treatment
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.
Citation	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; In press

Received	2025-09-05 08:55
Peer-Review Started	2025-09-05 08:55
To Make the First Decision
Return for Revision	2025-10-18 02:33
Revised	2025-10-28 11:37
Second Decision	2025-11-14 02:35
Accepted by Journal Editor-in-Chief
Accepted by Executive Editor-in-Chief	2025-11-14 08:50
Articles in Press	2025-11-14 08:50
Publication Fee Transferred	2025-11-02 04:06
Edit the Manuscript by Language Editor
Typeset the Manuscript

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