The role and mechanism of macrophage-to-myofibroblast transition in fibrotic diseases
- 1State Key Laboratory of Respiratory Disease, National Clinical Research Center for Respiratory Disease, National Center for Respiratory Medicine, Guangzhou Institute of Respiratory Health, The First Affiliated Hospital of Guangzhou Medical University
- 2Guangzhou National Laboratory, Bio-island
Abstract
Fibrosis is a pathological process primarily characterized by excessive deposition of extracellular matrix (ECM), which leads to disruption of tissue architecture and progressive loss of organ function, serving as a key pathological basis for various chronic diseases. Recent studies have revealed that, in addition to conventional sources, macrophages can directly differentiate into ECM-producing myofibroblasts through a process termed macrophage-to-myofibroblast transition (MMT), thereby actively participating in fibrogenesis. The concept of MMT was initially proposed in the context of renal fibrosis and has since been validated in multiple organs, including the kidney, heart, lung, liver, and retina. This review aims to summarize the role of MMT in fibrotic diseases and to elucidate the mechanism underlying MMT and fibrosis progression. Unlike prior reviews that predominantly focus on MMT within individual organs or separately delineate their molecular pathways, this review adopts a cross-organ perspective to systematically identify conserved mechanisms, tissue-specific regulatory networks, and translational challenges of MMT across fibrotic diseases.
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BibTeX
@article{guo2026role,
title = {{The role and mechanism of macrophage-to-myofibroblast transition in fibrotic diseases}},
author = {Hua Guo and Xiao Xiao Tang},
journal = {Frontiers in Immunology},
year = {2026},
month = oct,
doi = {10.3389/fimmu.2026.1919029},
url = {https://www.frontiersin.org/articles/10.3389/fimmu.2026.1919029/full},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - The role and mechanism of macrophage-to-myofibroblast transition in fibrotic diseases
AU - Hua Guo
AU - Xiao Xiao Tang
PY - 2026
DA - 2026/10/05
JO - Frontiers in Immunology
DO - 10.3389/fimmu.2026.1919029
UR - https://www.frontiersin.org/articles/10.3389/fimmu.2026.1919029/full
AB - Fibrosis is a pathological process primarily characterized by excessive deposition of extracellular matrix (ECM), which leads to disruption of tissue architecture and progressive loss of organ function, serving as a key pathological basis for various chronic diseases. Recent studies have revealed that, in addition to conventional sources, macrophages can directly differentiate into ECM-producing myofibroblasts through a process termed macrophage-to-myofibroblast transition (MMT), thereby actively participating in fibrogenesis. The concept of MMT was initially proposed in the context of renal fibrosis and has since been validated in multiple organs, including the kidney, heart, lung, liver, and retina. This review aims to summarize the role of MMT in fibrotic diseases and to elucidate the mechanism underlying MMT and fibrosis progression. Unlike prior reviews that predominantly focus on MMT within individual organs or separately delineate their molecular pathways, this review adopts a cross-organ perspective to systematically identify conserved mechanisms, tissue-specific regulatory networks, and translational challenges of MMT across fibrotic diseases.
SN - 1664-3224
ER -