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Mitochondrial dysfunction is emerging as a critical pathogenic driver, often occurring before cytokine release and trypsin activation. It links calcium overload, inflammatory signaling, permeability transition pore opening, mitophagy damage, and pancreatic cell injury. This review systematically analyzes mitochondria’s regulation of pancreatic homeostasis and evaluates novel strategies to mitigate mitochondrial dysfunction, supporting translational advances for improved AP diagnostics and mechanism-based treatment.",{"@graph":69,"@context":122},[70,84,105],{"@type":71,"itemListElement":72},"BreadcrumbList",[73,77,79,82],{"item":74,"name":75,"@type":76,"position":8},"https://docshare.wps.com","Home","ListItem",{"item":78,"name":9,"@type":76,"position":14},"https://docshare.wps.com/document/",{"item":80,"name":35,"@type":76,"position":81},"https://docshare.wps.com/document/healthcare/",3,{"item":83,"name":65,"@type":76,"position":19},"https://docshare.wps.com/document/mitochondrial-dysfunction-as-a-bridge-to-pathology-in-acute-pancreatitis-from-molecular-insights-to-novel-therapeutic-strategies/406435/",{"url":83,"name":65,"@type":85,"image":86,"author":91,"headline":65,"publisher":94,"fileFormat":97,"inLanguage":63,"description":67,"dateModified":98,"datePublished":99,"encodingFormat":97,"isAccessibleForFree":100,"interactionStatistic":101},"DigitalDocument",{"url":87,"@type":88,"width":89,"height":90},"https://docshare.wps.com/thumbnails/mitochondrial-dysfunction-as-a-bridge-to-pathology-in-acute-pancreatitis-from-molecular-insights-to-novel-therapeutic-strategies/406435.png","ImageObject",300,407,{"name":92,"@type":93},"Adam","Person",{"url":74,"name":95,"@type":96},"DocShare","Organization","application/pdf","2026-10-31","2026-09-28",true,{"@type":102,"interactionType":103,"userInteractionCount":34},"InteractionCounter",{"@type":104},"ViewAction",{"@type":106,"mainEntity":107},"FAQPage",[108,114,118],{"name":109,"@type":110,"acceptedAnswer":111},"What triggers acute pancreatitis in the article’s overview?","Question",{"text":112,"@type":113},"Acute pancreatitis is described as being triggered by premature activation of trypsin, leading to a dysregulated intra-pancreatic cascade and pancreatic tissue injury.","Answer",{"name":115,"@type":110,"acceptedAnswer":116},"How does mitochondrial dysfunction relate to the progression of acute pancreatitis?",{"text":117,"@type":113},"Mitochondrial dysfunction is presented as an early pathogenic driver that can precede both cytokine release and trypsin activation, contributing to calcium overload, inflammation, permeability transition pore opening, mitophagy damage, and cell injury.",{"name":119,"@type":110,"acceptedAnswer":120},"What is the main purpose of the review?",{"text":121,"@type":113},"The review aims to provide a comprehensive analysis of mitochondrial roles in regulating pancreatic homeostasis and to evaluate emerging therapeutic strategies targeting mitochondrial dysfunction to enable more mechanism-driven precision medicine.","https://schema.org",{"og:url":83,"og:type":124,"og:title":65,"og:site_name":95,"og:description":67},"article",{"robots":126,"canonical":83},"index,follow",{"doc_id":128,"site_id":62},406435,1790818574,{"code":4,"msg":5,"data":131},{"doc_id":128,"user_id":132,"nickname":92,"user_avatar":133,"doc_module":4,"category_id":34,"category_name":35,"doc_title":65,"doc_description":67,"doc_content":134,"file_id":135,"file_url":136,"file_type":137,"file_size":138,"view_count":34,"is_deleted":4,"is_public":8,"is_downloadable":8,"audit_status":8,"page_count":139,"language":140,"language_code":63,"site_id":62,"html_lang":63,"table_of_contents":141,"faqs":142,"seo_title":143,"seo_description":67,"update_tm":144,"read_time":36,"preview_page_count":4},1374404737137,"https://ap-avatar.wpscdn.com/davatar_155a257f0dc6eb9ab79c44ca47cae57d","| W | J | G | World Journal of\u003Cbr>Gastroenterology |\n| --- | --- | --- | --- |\n\nSubmit a Manuscript: [https://www.f6publishing.com](https://www.f6publishing.com) World J Gastroenterol 2025 December 28; 31(48): 113840  \nDOI: 10.3748/wjg.v31.i48.113840 ISSN 1007-9327 (print) ISSN 2219-2840 (online)  \nREVIEW  \nMitochondrial dysfunction as a bridge to pathology in acute  \npancreatitis: From molecular insights to novel therapeutic strategies  \nChuan-Chao Xia, Yue Xu, Zhen-Huan Wang, Guo-Qiang Xu  \nSpecialty type: Gastroenterology and hepatology  \nProvenance and peer review:  \nUnsolicited article; Externally peer reviewed.  \nPeer-review model: Single blind  \nPeer-review report’s classification Scientific Quality: Grade A, Grade A, Grade B, Grade C  \nNovelty: Grade A, Grade B, Grade B, Grade B  \nCreativity or Innovation: Grade B, Grade B, Grade B, Grade B Scientific Significance: Grade A, Grade A, Grade B, Grade B  \nP-Reviewer: Valencia ED, Professor, Colombia; Zhang XB, China; Zhao GD, PhD, Associate Professor, China  \nReceived: September 5, 2025  \nRevised: October 28, 2025  \nAccepted: November 14, 2025  \nPublished online: December 28, 2025  \nProcessing time: 113 Days and 19.6 Hours  \nChuan-Chao Xia, Yue Xu, Guo-Qiang Xu, Department of Gastroenterology, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310003, Zhejiang Province, China  \nZhen-Huan Wang, Department of Radiology, The Second Affiliated Hospital of Naval Medical University, Shanghai 200003, China  \nCo-first authors: Chuan-Chao Xia and Yue Xu.  \nCo-corresponding authors: Zhen-Huan Wang and Guo-Qiang Xu.  \nCorresponding 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.](China. 1193065@zju.edu.cn)[ 1193065@zju.edu.cn](China. 1193065@zju.edu.cn)  \nAbstract  \nAcute 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 cuttingedge research findings, this work highlights the translational potential of these advancements in redefining diagnostic frameworks and optimizing therapeutic approaches for the management of AP.  \nKey Words: Acute pancreatitis; Mitochondria; Mitochondrial dysfunction; Molecular mechanism; Treatment  \n©The Author(s) 2025. Published by Baishideng Publishing Group Inc. All rights reserved.  \n WJG  [https://www.wjgnet.com](https://www.wjgnet.com) 1 December 28, 2025  Volume 31  Issue 48   \nXia CC et al. Mitochondrial dysfunction in AP  \nCore 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 t","cbCaid7uCGnwR6Ch","https://ap.wps.com/l/cbCaid7uCGnwR6Ch","pdf",1198625,16,"English","# Core Tip\n# Abstract\n# Key Words\n# Introduction\n## Pathophysiological cascade and severity categories\n## Biochemical hallmarks and diagnostic considerations","[{\"question\":\"What triggers acute pancreatitis in the article’s overview?\",\"answer\":\"Acute pancreatitis is described as being triggered by premature activation of trypsin, leading to a dysregulated intra-pancreatic cascade and pancreatic tissue injury.\"},{\"question\":\"How does mitochondrial dysfunction relate to the progression of acute pancreatitis?\",\"answer\":\"Mitochondrial dysfunction is presented as an early pathogenic driver that can precede both cytokine release and trypsin activation, contributing to calcium overload, inflammation, permeability transition pore opening, mitophagy damage, and cell injury.\"},{\"question\":\"What is the main purpose of the review?\",\"answer\":\"The review aims to provide a comprehensive analysis of mitochondrial roles in regulating pancreatic homeostasis and to evaluate emerging therapeutic strategies targeting mitochondrial dysfunction to enable more mechanism-driven precision medicine.\"}]","Mitochondrial dysfunction as a bridge to pathology in acute pancreatitis - From molecular insights to novel therapeutic strategies | PDF",1790565652]