Research progress on the role and mechanism of 5-hydroxytryptamine and M2 macrophages in pulmonary interstitial fibrosis.
10.3760/cma.j.cn121430-20230724-00549
- Author:
Yiming DENG
1
;
Changwen DENG
;
Xiaoping ZHU
Author Information
1. Department of Respiratory and Critical Care Medicine, East Hospital, Tongji University, Shanghai 200120, China. Corresponding author: Zhu Xiaoping, Email: z_xping@hotmail.com.
- Publication Type:Journal Article
- MeSH:
Humans;
Serotonin;
Macrophages;
Lung Diseases, Interstitial/pathology*;
Lung/pathology*;
Idiopathic Pulmonary Fibrosis;
Fibrosis
- From:
Chinese Critical Care Medicine
2023;35(9):1004-1008
- CountryChina
- Language:Chinese
-
Abstract:
Idiopathic pulmonary fibrosis (IPF) is a progressive and fatal interstitial lung disease, the cause is not yet clear. Pathological manifestations are abnormal repair changes resulting from sustained lung injury. Macrophages have been identified as playing a key role in IPF pathogenesis. In different local microenvironments, macrophages can exhibit either classically activated (M1) or alternately activated (M2) phenotypes. M1 plays a key role in promoting inflammatory response and is involved in the process of causing alveolar tissue injury. M2 is involved in wound healing and stopping lung inflammation. Previous studies have shown that activation of 5-hydroxytryptamine (5-HT) signaling is enhanced in pulmonary fibrosis and that 5-HT receptors play an important role in the observed pro-fibrotic effects. As a multifunctional signaling molecule, 5-HT is closely related to lung macrophage polarization, early lung tissue injury, abnormal proliferation and repair, and late extracellular matrix (ECM) deposition. This article reviewed the role of 5-HT and M2 macrophages in the pathogenesis of IPF and the possible regulatory mechanism of 5-HT, in order to provide a reference for further research.
