ReviewReviews in cardiovascular medicine2026
MMT: A Potential Mechanism of Myocardial Fibrosis - Regulation of the TGF-β1/Smad3 Pathway and Prospects for Targeted Therapy.
Review in Reviews in cardiovascular medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Authors and funding
6 authors.
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Abstract
Macrophage-Myofibroblast Transition (MMT) is a process in which macrophages, under the influence of specific factors such as transforming growth factor-beta 1 (TGF-β1) within a fibrotic microenvironment, gradually lose their original immune phenotype and acquire the biological characteristics of myofibroblasts. This transition involves changes in cell morphology, protein expression, and function, representing an important mechanism in the development and progression of tissue fibrosis. The TGF-β1/Smad3 signaling pathway, as a central regulator of fibrosis, plays a key role in MMT by modulating cell proliferation, differentiation, and the synthesis and degradation of extracellular matrix. Recent studies have identified MMT as a newly recognized form of phenotypic switching that contributes significantly to fibrosis in multiple organs, including the heart, lungs, liver, and kidneys. Experimental evidence has confirmed that the TGF-β1/Smad3 pathway directly regulates critical steps in MMT, thereby promoting the progression of fibrosis. However, the specific molecular targets and detailed mechanisms underlying this regulation remain incompletely understood and require further investigation. Elucidating the regulatory network of this pathway may offer new strategies for early intervention and targeted therapy in clinical diseases with fibrosis. However, direct evidence for MMT in human myocardial fibrosis remains limited, and its relative contribution compared to other sources of myofibroblasts requires further elucidation.
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