Abstract |
Acute pancreatitis (AP) is an inflammatory disease characterized by acute inflammation and necrosis of the pancreatic parenchyma. AP is often associated with organ failure, sepsis, and high mortality. The pathogenesis of AP is still not well understood. In recent years several papers have highlighted the cellular and molecular events of acute pancreatitis. Pancreatitis is initiated by activation of digestive enzymes within the acinar cells that are involved in autodigestion of the gland, followed by a massive infiltration of neutrophils and macrophages and release of inflammatory mediators, responsible for the local and systemic inflammatory response. The hallmark of AP is parenchymal cell necrosis that represents the cause of the high morbidity and mortality, so that new potential therapeutic approaches are indispensable for the treatment of patients at high risk of complications. However, not all factors that determine the onset and course of the disease have been explained. Aim of this article is to review the role of mitogen-activated protein kinases in pathogenesis of acute pancreatitis.
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Authors | Natasha Irrera, Alessandra Bitto, Monica Interdonato, Francesco Squadrito, Domenica Altavilla |
Journal | World journal of gastroenterology
(World J Gastroenterol)
Vol. 20
Issue 44
Pg. 16535-43
(Nov 28 2014)
ISSN: 2219-2840 [Electronic] United States |
PMID | 25469021
(Publication Type: Journal Article, Review)
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Chemical References |
- Anti-Inflammatory Agents
- Protein Kinase Inhibitors
- Mitogen-Activated Protein Kinases
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Topics |
- Acute Disease
- Animals
- Anti-Inflammatory Agents
(pharmacology)
- Disease Models, Animal
- Enzyme Activation
- Humans
- MAP Kinase Signaling System
(drug effects)
- Mitogen-Activated Protein Kinases
(antagonists & inhibitors, metabolism)
- Molecular Targeted Therapy
- Pancreas
(drug effects, enzymology, immunology, pathology)
- Pancreatitis
(diagnosis, drug therapy, enzymology, immunology)
- Protein Kinase Inhibitors
(pharmacology)
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