Abstract

Pancreatitis is increasingly recognized as not merely a local inflammation of the pancreas but also a disease with high frequency of systemic sequelae. Current understanding of the cellular mechanisms that trigger it and affect the development of sequelae are limited. Genetically engineered mouse models can be a useful tool to study the pathophysiology of pancreatitis. This article gives an overview of the genetically engineered mouse models that spontaneously develop pancreatitis and discusses those that most closely replicate different pancreatitis hallmarks observed in humans.

Highlights

  • Standardization for management of acute significant overall progress has development of metabolic disorders, such as exocrine been made during the last few decades (evidenced by a pancrDeeadtiiccatiendstuofPfiacuiel Pnlcayceh(EoPldIe)r, post-pancreatitis diabetes reduction in mortality rates), the improved outcomes mellitus (PPDM), and ectopic fat accumulation in the have not been due to any treatments based on specific pancreas [3,4,5,6]

  • Depending on the administration strategy employed this can resemble many of the common characteristics of human pancreatitis, including aberrant zymogen activation in the acinar cell, impaired exocrine pancreatic secretion, inflammation, morphological abnormalities, fibrosis and trans-differentiation of acini [13, 14]

  • An alternative approach that may be more specific to the underlying pathophysiology causing pancreatitis is the adoption of genetic mouse models

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Summary

Open Access

Journal xyz 2017; 1 (2): 122–135 genetically engineered mouse models (GEMM) that may be used to study the pancreatitis phenotype, with particular. AbstrTachte: PFairnsctreDateitcisadisein(1cr9e6as4in-1g9ly7r2ec)ognized as not focus on those that show hallmarks of the humans. MerelRyeaseloacracl hinAflarmticmlaetion of the pancreas and a disease with high frequency of systemic sequelae. 25, 2013; published on-linmeiJludly, 1m2,o2d0e14rate, severe, and critical) is useful for the clinical assessment of severity in individual patients

Thisswwoorrkkisis licensed under the Creative Commons
GEMM of pancreatitis
Trypsinogen hereditary models
Transgenic over Pancreatic
In general appears normal
Timedependent global Global
Inflammation and cytokines
Pancreatic acinar cells Global
Acini immune cell infiltration
Pancreatic acinar cells
Transcription factor Double knockout Global
Iron uptake
Lipid and glucose Knockout
Genetic disease models that present with pancreatitis
ER stress and autophagy
Summary
Full Text
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