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      Mitochondrial dysfunction in pancreatic acinar cells: mechanisms and therapeutic strategies in acute pancreatitis

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          Abstract

          Acute pancreatitis (AP) is an inflammatory disease of the pancreas and a complex process involving multiple factors, with mitochondrial damage playing a crucial role. Mitochondrial dysfunction is now considered a key driver in the development of AP. This dysfunction often presents as increased oxidative stress, altered membrane potential and permeability, and mitochondrial DNA damage and mutations. Under stress conditions, mitochondrial dynamics and mitochondrial ROS production increase, leading to decreased mitochondrial membrane potential, imbalanced calcium homeostasis, and activation of the mitochondrial permeability transition pore. The release of mitochondrial DNA (mtDNA), recognized as damage-associated molecular patterns, can activate the cGAS-STING1 and NF-κB pathway and induce pro-inflammatory factor expression. Additionally, mtDNA can activate inflammasomes, leading to interleukin release and subsequent tissue damage and inflammation. This review summarizes the relationship between mitochondria and AP and explores mitochondrial protective strategies in the diagnosis and treatment of this disease. Future research on the treatment of acute pancreatitis can benefit from exploring promising avenues such as antioxidants, mitochondrial inhibitors, and new therapies that target mitochondrial dysfunction.

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          Most cited references230

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          Classification of acute pancreatitis--2012: revision of the Atlanta classification and definitions by international consensus.

          The Atlanta classification of acute pancreatitis enabled standardised reporting of research and aided communication between clinicians. Deficiencies identified and improved understanding of the disease make a revision necessary. A web-based consultation was undertaken in 2007 to ensure wide participation of pancreatologists. After an initial meeting, the Working Group sent a draft document to 11 national and international pancreatic associations. This working draft was forwarded to all members. Revisions were made in response to comments, and the web-based consultation was repeated three times. The final consensus was reviewed, and only statements based on published evidence were retained. The revised classification of acute pancreatitis identified two phases of the disease: early and late. Severity is classified as mild, moderate or severe. Mild acute pancreatitis, the most common form, has no organ failure, local or systemic complications and usually resolves in the first week. Moderately severe acute pancreatitis is defined by the presence of transient organ failure, local complications or exacerbation of co-morbid disease. Severe acute pancreatitis is defined by persistent organ failure, that is, organ failure >48 h. Local complications are peripancreatic fluid collections, pancreatic and peripancreatic necrosis (sterile or infected), pseudocyst and walled-off necrosis (sterile or infected). We present a standardised template for reporting CT images. This international, web-based consensus provides clear definitions to classify acute pancreatitis using easily identified clinical and radiologic criteria. The wide consultation among pancreatologists to reach this consensus should encourage widespread adoption.
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            Biological Functions of Autophagy Genes: A Disease Perspective

            The lysosomal degradation pathway of autophagy plays a fundamental role in cellular, tissue, and organismal homeostasis and is mediated by evolutionarily conserved autophagy-related (ATG) genes. Definitive etiological links exist between mutations in genes that control autophagy and human disease, especially neurodegenerative, inflammatory disorders and cancer. Autophagy selectively targets dysfunctional organelles, intracellular microbes, and pathogenic proteins, and deficiencies in these processes may lead to disease. Moreover, ATG genes have diverse physiologically important roles in other membrane-trafficking and signaling pathways. This Review discusses the biological functions of autophagy genes from the perspective of understanding-and potentially reversing-the pathophysiology of human disease and aging.
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              Autophagy in the pathogenesis of disease.

              Autophagy is a lysosomal degradation pathway that is essential for survival, differentiation, development, and homeostasis. Autophagy principally serves an adaptive role to protect organisms against diverse pathologies, including infections, cancer, neurodegeneration, aging, and heart disease. However, in certain experimental disease settings, the self-cannibalistic or, paradoxically, even the prosurvival functions of autophagy may be deleterious. This Review summarizes recent advances in understanding the physiological functions of autophagy and its possible roles in the causation and prevention of human diseases.
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                Author and article information

                Contributors
                URI : https://loop.frontiersin.org/people/2854399Role: Role:
                URI : https://loop.frontiersin.org/people/2925124Role: Role:
                URI : https://loop.frontiersin.org/people/2418758Role: Role: Role: Role:
                URI : https://loop.frontiersin.org/people/2924993Role: Role:
                URI : https://loop.frontiersin.org/people/2924986Role: Role:
                URI : https://loop.frontiersin.org/people/1844462Role: Role:
                URI : https://loop.frontiersin.org/people/2924966Role: Role: Role: Role:
                URI : https://loop.frontiersin.org/people/1494240Role: Role: Role: Role:
                Journal
                Front Immunol
                Front Immunol
                Front. Immunol.
                Frontiers in Immunology
                Frontiers Media S.A.
                1664-3224
                24 December 2024
                2024
                : 15
                : 1503087
                Affiliations
                [1] 1 Department of Hepatobiliary Surgery, The First Affiliated Hospital of Xi’an Jiaotong University , Xi’an, China
                [2] 2 Pancreatic Disease Center of Xi’an Jiaotong University , Xi’an, China
                [3] 3 Center for Translational Medicine, The First Affiliated Hospital of Xi’an Jiaotong University , Xi’an, China
                Author notes

                Edited by: Jiaheng Xie, Central South University, China

                Reviewed by: Chunying Li, Georgia State University, United States

                Yan Shen, Chongqing University of Technology, China

                *Correspondence: Fang Cao, Lanching@ 123456xjtu.edu.cn ; Zhenhua Ma, mzh@ 123456xjtu.edu.cn

                †These authors have contributed equally to this work

                Article
                10.3389/fimmu.2024.1503087
                11703726
                39776917
                5aa445c2-298f-49e9-8e60-bc74d7cff845
                Copyright © 2024 Chen, Xu, Han, Ding, Ren, Wang, Ma and Cao

                This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

                History
                : 28 September 2024
                : 09 December 2024
                Page count
                Figures: 6, Tables: 0, Equations: 0, References: 230, Pages: 21, Words: 10920
                Funding
                Funded by: National Natural Science Foundation of China , doi 10.13039/501100001809;
                Award ID: 82173365, 82072699
                The author(s) declare financial support was received for the research, authorship, and/or publication of this article. This study was funded by the National Natural Science Foundation of China (No.82072699 and 82173365).
                Categories
                Immunology
                Review
                Custom metadata
                Inflammation

                Immunology
                acute pancreatitis,mitochondrial,calcium overload,mitochondrial permeability transition pore,regulated cell death

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