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The Pivotal Role of Macrophages in the Pathogenesis of Pancreatic Diseases.
Ryu, Seungyeon; Lee, Eun Kyung.
Afiliação
  • Ryu S; Department of Biochemistry, College of Medicine, The Catholic University of Korea, Seoul 06591, Republic of Korea.
  • Lee EK; Department of Biomedicine & Health Sciences, College of Medicine, The Catholic University of Korea, Seoul 06591, Republic of Korea.
Int J Mol Sci ; 25(11)2024 May 25.
Article em En | MEDLINE | ID: mdl-38891952
ABSTRACT
The pancreas is an organ with both exocrine and endocrine functions, comprising a highly organized and complex tissue microenvironment composed of diverse cellular and non-cellular components. The impairment of microenvironmental homeostasis, mediated by the dysregulation of cell-to-cell crosstalk, can lead to pancreatic diseases such as pancreatitis, diabetes, and pancreatic cancer. Macrophages, key immune effector cells, can dynamically modulate their polarization status between pro-inflammatory (M1) and anti-inflammatory (M2) modes, critically influencing the homeostasis of the pancreatic microenvironment and thus playing a pivotal role in the pathogenesis of the pancreatic disease. This review aims to summarize current findings and provide detailed mechanistic insights into how alterations mediated by macrophage polarization contribute to the pathogenesis of pancreatic disorders. By analyzing current research comprehensively, this article endeavors to deepen our mechanistic understanding of regulatory molecules that affect macrophage polarity and the intricate crosstalk that regulates pancreatic function within the microenvironment, thereby facilitating the development of innovative therapeutic strategies that target perturbations in the pancreatic microenvironment.
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Texto completo: 1 Base de dados: MEDLINE Assunto principal: Macrófagos Limite: Animals / Humans Idioma: En Ano de publicação: 2024 Tipo de documento: Article

Texto completo: 1 Base de dados: MEDLINE Assunto principal: Macrófagos Limite: Animals / Humans Idioma: En Ano de publicação: 2024 Tipo de documento: Article