Department of Biochemistry, College of Medicine, The Catholic University of Korea, Seoul 06591, Republic of Korea.
Department of Biomedicine & Health Sciences, College of Medicine, The Catholic University of Korea, Seoul 06591, Republic of Korea.
Int J Mol Sci. 2024 May 25;25(11):5765. doi: 10.3390/ijms25115765.
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.
胰腺是一个具有外分泌和内分泌功能的器官，由高度组织化和复杂的组织微环境组成，其中包含多种细胞和非细胞成分。细胞间通讯失调介导的微环境稳态失调可导致胰腺炎、糖尿病和胰腺癌等胰腺疾病。巨噬细胞作为关键的免疫效应细胞，可以在促炎（M1）和抗炎（M2）两种极化状态之间动态调节其极化状态，对胰腺微环境的稳态具有重要影响，因此在胰腺疾病的发病机制中发挥关键作用。本综述旨在总结当前的研究发现，并详细阐述巨噬细胞极化介导的改变如何促进胰腺疾病的发病机制。通过全面分析当前的研究，本文旨在深入了解影响巨噬细胞极性的调节分子以及调节微环境中胰腺功能的复杂细胞间通讯，从而为靶向胰腺微环境中扰动的创新治疗策略的发展提供帮助。
