Overview of the cellular and immune mechanisms involved in acute pancreatitis: In search of new prognosis biomarkers

Acute pancreatitis (AP) is an acute-onset gastrointestinal disease characterized by a significant inflammation of the pancreas. Most of the time, AP does not leave substantial changes in the pancreas after the resolution of the symptoms but the severe forms are associated with local or systemic comp...

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Main Authors: Alexandra Mititelu, Alina Grama, Marius-Cosmin Colceriu, Tudor L. Pop
Format: Article
Language:English
Published: Cambridge University Press 2025-01-01
Series:Expert Reviews in Molecular Medicine
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Online Access:https://www.cambridge.org/core/product/identifier/S1462399424000401/type/journal_article
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author Alexandra Mititelu
Alina Grama
Marius-Cosmin Colceriu
Tudor L. Pop
author_facet Alexandra Mititelu
Alina Grama
Marius-Cosmin Colceriu
Tudor L. Pop
author_sort Alexandra Mititelu
collection DOAJ
description Acute pancreatitis (AP) is an acute-onset gastrointestinal disease characterized by a significant inflammation of the pancreas. Most of the time, AP does not leave substantial changes in the pancreas after the resolution of the symptoms but the severe forms are associated with local or systemic complications. The pathogenesis of AP has long been investigated and, lately, the importance of intracellular mechanisms and the immune system has been described. The initial modifications in AP take place in the acinar cell. There are multiple mechanisms by which cellular homeostasis is impaired, one of the most important being calcium overload. Necrotic pancreatic cells initiate the inflammatory response by secreting inflammatory mediators and attracting immune cells. From this point on, the inflammation is sustained by the involvement of innate and adaptive immune systems. Multiple studies have demonstrated the importance of the first 48 h for identifying patients at risk for developing severe forms. For this reason, there is a need to find new, easy-to-use and reliable markers for accurate predictions of these forms. This review provides an overview of the main pathogenetic mechanisms involved in AP development and the most promising biomarkers for severity stratification.
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spelling doaj-art-a3130a5d528747beab257c9e85d470912025-08-20T12:57:28ZengCambridge University PressExpert Reviews in Molecular Medicine1462-39942025-01-012710.1017/erm.2024.40Overview of the cellular and immune mechanisms involved in acute pancreatitis: In search of new prognosis biomarkersAlexandra Mititelu0https://orcid.org/0000-0002-0955-4486Alina Grama1https://orcid.org/0000-0001-7022-6345Marius-Cosmin Colceriu2https://orcid.org/0009-0001-8023-2631Tudor L. Pop3https://orcid.org/0000-0002-4931-12192nd Pediatric Discipline, Department of Mother and Child, Iuliu Hatieganu University of Medicine and Pharmacy, Cluj-Napoca, Romania2nd Pediatric Discipline, Department of Mother and Child, Iuliu Hatieganu University of Medicine and Pharmacy, Cluj-Napoca, Romania 2nd Pediatric Clinic, Emergency Clinical Hospital for Children, Cluj-Napoca, Romania2nd Pediatric Discipline, Department of Mother and Child, Iuliu Hatieganu University of Medicine and Pharmacy, Cluj-Napoca, Romania2nd Pediatric Discipline, Department of Mother and Child, Iuliu Hatieganu University of Medicine and Pharmacy, Cluj-Napoca, Romania 2nd Pediatric Clinic, Emergency Clinical Hospital for Children, Cluj-Napoca, RomaniaAcute pancreatitis (AP) is an acute-onset gastrointestinal disease characterized by a significant inflammation of the pancreas. Most of the time, AP does not leave substantial changes in the pancreas after the resolution of the symptoms but the severe forms are associated with local or systemic complications. The pathogenesis of AP has long been investigated and, lately, the importance of intracellular mechanisms and the immune system has been described. The initial modifications in AP take place in the acinar cell. There are multiple mechanisms by which cellular homeostasis is impaired, one of the most important being calcium overload. Necrotic pancreatic cells initiate the inflammatory response by secreting inflammatory mediators and attracting immune cells. From this point on, the inflammation is sustained by the involvement of innate and adaptive immune systems. Multiple studies have demonstrated the importance of the first 48 h for identifying patients at risk for developing severe forms. For this reason, there is a need to find new, easy-to-use and reliable markers for accurate predictions of these forms. This review provides an overview of the main pathogenetic mechanisms involved in AP development and the most promising biomarkers for severity stratification.https://www.cambridge.org/core/product/identifier/S1462399424000401/type/journal_articleacute pancreatitisbiomarkersimmune systempathogenesisprognosticseverity
spellingShingle Alexandra Mititelu
Alina Grama
Marius-Cosmin Colceriu
Tudor L. Pop
Overview of the cellular and immune mechanisms involved in acute pancreatitis: In search of new prognosis biomarkers
Expert Reviews in Molecular Medicine
acute pancreatitis
biomarkers
immune system
pathogenesis
prognostic
severity
title Overview of the cellular and immune mechanisms involved in acute pancreatitis: In search of new prognosis biomarkers
title_full Overview of the cellular and immune mechanisms involved in acute pancreatitis: In search of new prognosis biomarkers
title_fullStr Overview of the cellular and immune mechanisms involved in acute pancreatitis: In search of new prognosis biomarkers
title_full_unstemmed Overview of the cellular and immune mechanisms involved in acute pancreatitis: In search of new prognosis biomarkers
title_short Overview of the cellular and immune mechanisms involved in acute pancreatitis: In search of new prognosis biomarkers
title_sort overview of the cellular and immune mechanisms involved in acute pancreatitis in search of new prognosis biomarkers
topic acute pancreatitis
biomarkers
immune system
pathogenesis
prognostic
severity
url https://www.cambridge.org/core/product/identifier/S1462399424000401/type/journal_article
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