ArticleEuropean journal of medical research2023
Role of macrophage-to-myofibroblast transition in chronic liver injury and liver fibrosis.
Article in European journal of medical research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 26 citations in OpenAlex.
- MMT: A Potential Mechanism of Myocardial Fibrosis - Regulation of the TGF-β1/Smad3 Pathway and Prospects for Targeted Therapy.Reviews in cardiovascular medicine · 2026Review
- Macrophage regulation of extracellular matrix remodeling in aging skeletal muscle.Ageing research reviews · 2026Review
- MFAP4 Promotes Scar Formation by Regulating Macrophage-Myofibroblast Transformation Through Activation of the TGF-β/Smad3 Signalling Pathway.Experimental dermatology · 2026Article
- Dapagliflozin attenuates diabetic renal fibrosis by inhibiting macrophage-myofibroblast transitionPeerJ · 2026Article
- Extracellular matrix stiffness in hepatocellular carcinoma: mechanisms and targeted therapeutic strategies.Frontiers in immunology · 2026Review
- Granzyme B contributes to subretinal fibrosis in neovascular age-related macular degeneration by modulating inflammation and epithelial-mesenchymal transition.Journal of neuroinflammation · 2025Article
- UCP2 Upregulates ACSL3 to Enhance Lipid Droplet Release from Acinar Cells and Modulates the Sirt1/Smad3 Pathway to Promote Macrophage-to-Myofibroblast Transition in Chronic Pancreatitis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Macrophage transition to a myofibroblast state drives fibrotic disease in uropathogenic E. coli-induced epididymo-orchitis.The Journal of clinical investigation · 2025Article
- Non-coding RNAs in alcohol-associated liver disease.Liver research (Beijing, China) · 2025Review
- PGC-1α mediates migrasome secretion accelerating macrophage-myofibroblast transition and contributing to sepsis-associated pulmonary fibrosis.Experimental & molecular medicine · 2025Article
- Pathological Changes in Extracellular Matrix Composition Orchestrate the Fibrotic Feedback Loop Through Macrophage Activation in Dupuytren's Contracture.International journal of molecular sciences · 2025Article
- Role of triggering receptor expressed on myeloid cells 2 in the pathogenesis of non-alcoholic fatty liver disease.World journal of hepatology · 2025Review
- EZH2-mediated macrophage-to-myofibroblast transition contributes to calcium oxalate crystal-induced kidney fibrosis.Communications biology · 2025Article
- Effect of macrophage-to-myofibroblast transition on silicosis.Animal models and experimental medicine · 2025Article
- Correlation between differences in the intestinal flora structure and Chinese medicine evidence in patients with Wilson disease-related liver fibrosis analyzed via high-throughput sequencing technology.Bioscience of microbiota, food and health · 2025Article
- Targeting Smad3 Phosphorylation Attenuates Anastomotic Intimal Hyperplasia and Perigraft Fibrosis in Decellularized Tissue-Engineered Vascular Grafts.Biomaterials research · 2025Article
- Targeting macrophage-myofibroblast transition withFrontiers in pharmacology · 2025Article
- The role of macrophages in hypertrophic scarring: molecular to therapeutic insights.Frontiers in immunology · 2025Review
- Exosomes From Human Umbilical Cord Stem Cells Suppress Macrophage-to-myofibroblast Transition, Alleviating Renal Fibrosis.Inflammation · 2024Article
- ADAM8 promotes alcoholic liver fibrosis through the MAPK signaling pathway.The journal of physiological sciences : JPS · 2024Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundChronic liver injury contributes to liver fibrosis, which is characterized by the excessive deposition of extracellular matrix (ECM) components. ECM is mainly composed of myofibroblasts. Recently, macrophage-to-myofibroblasts transition (MMT), has been identified as a novel origin for myofibroblasts. However, the potential functions of MMT in chronic liver injury and liver fibrosis remain unknown.
methodsTo clarify the transformation of fibrotic cells in hepatic fibrosis, liver specimens were collected from people at different stages in the progression of hepatic fibrosis and stained with immunofluorescence. Models of hepatic fibrosis such as the CCL4 model, HFD-induced NAFLD model, MCD-induced NAFLD model and ethanol-induced AFLD model were demonstrated and were stained with immunofluorescence.
resultsHere, we uncovered macrophages underwent MMT in clinical liver fibrosis tissue samples and multiple animal models of chronic liver injury. MMT cells were found in specimens from patients with liver fibrosis on the basis of co-expression of macrophage (CD68) and myofibroblast (a-SMA) markers. Moreover, macrophages could transform into myofibroblasts in CCL4-induced liver fibrosis model, high-fat diet (HFD) and methionine-choline-deficient diet (MCD)-induced nonalcoholic fatty liver diseases (NAFLD) model, and ethanol-induced alcoholic fatty liver diseases (AFLD) model. In addition, we highlighted that MMT cells mainly had a predominant M2 phenotype in both human and experimental chronic liver injury.
conclusionsTaken together, MMT acts a crucial role in chronic liver injury and liver fibrosis.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.