Key result
Macrophage-to-myofibroblast transition drives cross-organ fibrosis via the TGF-β1/Smad3 pathway in chronic inflammation.
Why the study?
Macrophage-to-myofibroblast transition (MMT) has been identified as a novel contributor to fibrogenesis across multiple organs, but a systematic cross-organ understanding of its role and mechanisms in fibrotic diseases is lacking.
Targeting macrophage-to-myofibroblast transition and its core signaling pathways represents a promising cross-organ therapeutic strategy for mitigating chronic fibrotic diseases.
MMT identifies a unified inflammatory-fibrotic target; leaves open whether TGF-β1/Smad3 blockade reverses established human disease.
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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Guo et al. (2026) conducted a review in Fibrotic diseases. Macrophage-to-myofibroblast transition (MMT) was evaluated. Macrophage-to-myofibroblast transition (MMT), primarily driven by the TGF-β1/Smad3 pathway, serves as a conserved cross-organ mechanism linking chronic inflammation to excessive extracellular matrix deposition.
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