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      New insights into the etiology, risk factors, and pathogenesis of pancreatitis in dogs: Potential impacts on clinical practice

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          Abstract

          While most cases of pancreatitis in dogs are thought to be idiopathic, potential risk factors are identified. In this article we provide a state‐of‐the‐art overview of suspected risk factors for pancreatitis in dogs, allowing for improved awareness and detection of potential dog‐specific risk factors, which might guide the development of disease prevention strategies. Additionally, we review important advances in our understanding of the pathophysiology of pancreatitis and potential areas for therapeutic manipulation based thereof. The outcome of pathophysiologic mechanisms and the development of clinical disease is dependent on the balance between stressors and protective mechanisms, which can be evaluated using the critical threshold theory.

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          Most cited references211

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          Mechanism and medical implications of mammalian autophagy

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            New insights into acute pancreatitis

            The incidence of acute pancreatitis continues to increase worldwide, and it is one of the most common gastrointestinal causes for hospital admission in the USA. In the past decade, substantial advancements have been made in our understanding of the pathophysiological mechanisms of acute pancreatitis. Studies have elucidated mechanisms of calcium-mediated acinar cell injury and death and the importance of store-operated calcium entry channels and mitochondrial permeability transition pores. The cytoprotective role of the unfolded protein response and autophagy in preventing sustained endoplasmic reticulum stress, apoptosis and necrosis has also been characterized, as has the central role of unsaturated fatty acids in causing pancreatic organ failure. Characterization of these pathways has led to the identification of potential molecular targets for future therapeutic trials. At the patient level, two classification systems have been developed to classify the severity of acute pancreatitis into prognostically meaningful groups, and several landmark clinical trials have informed management strategies in areas of nutritional support and interventions for infected pancreatic necrosis that have resulted in important changes to acute pancreatitis management paradigms. In this Review, we provide a summary of recent advances in acute pancreatitis with a special emphasis on pathophysiological mechanisms and clinical management of the disorder.
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              Mitochondrial Dysfunction, Through Impaired Autophagy, Leads to Endoplasmic Reticulum Stress, Deregulated Lipid Metabolism, and Pancreatitis in Animal Models.

              Little is known about the signaling pathways that initiate and promote acute pancreatitis (AP). The pathogenesis of AP has been associated with abnormal increases in cytosolic Ca2+, mitochondrial dysfunction, impaired autophagy, and endoplasmic reticulum (ER) stress. We analyzed the mechanisms of these dysfunctions and their relationships, and how these contribute to development of AP in mice and rats.
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                Author and article information

                Contributors
                cridgeh1@msu.edu
                Journal
                J Vet Intern Med
                J Vet Intern Med
                10.1111/(ISSN)1939-1676
                JVIM
                Journal of Veterinary Internal Medicine
                John Wiley & Sons, Inc. (Hoboken, USA )
                0891-6640
                1939-1676
                12 May 2022
                May-Jun 2022
                : 36
                : 3 ( doiID: 10.1111/jvim.v36.3 )
                : 847-864
                Affiliations
                [ 1 ] Department of Small Animal Clinical Sciences, College of Veterinary Medicine Michigan State University East Lansing Michigan USA
                [ 2 ] Gastrointestinal Laboratory, Department of Small Animal Clinical Sciences, College of Veterinary Medicine and Biomedical Sciences Texas A&M University Texas USA
                [ 3 ] Gastrointestinal Cancer and Inflammatory Research Laboratory Technical University of Munich Munich Germany
                Author notes
                [*] [* ] Correspondence

                Harry Cridge, Department of Small Animal Clinical Sciences, College of Veterinary Medicine, Michigan State University, East Lansing, MI, USA.

                Email: cridgeh1@ 123456msu.edu

                Author information
                https://orcid.org/0000-0003-0236-2307
                https://orcid.org/0000-0003-3336-2086
                Article
                JVIM16437
                10.1111/jvim.16437
                9151489
                35546513
                9347bfe2-27ce-4d25-a731-5553f12a61be
                © 2022 The Authors. Journal of Veterinary Internal Medicine published by Wiley Periodicals LLC on behalf of American College of Veterinary Internal Medicine.

                This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.

                History
                : 08 April 2022
                : 04 January 2022
                : 12 April 2022
                Page count
                Figures: 8, Tables: 1, Pages: 18, Words: 16983
                Categories
                Review
                Small Animal
                Review
                Endocrinology
                Custom metadata
                2.0
                May/June 2022
                Converter:WILEY_ML3GV2_TO_JATSPMC version:6.1.6 mode:remove_FC converted:30.05.2022

                Veterinary medicine
                colocalization,critical threshold theory,er stress,impaired autophagy,mitochondrial dysfunction,oxidative stress,pathologic calcium signaling

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