ArticleThe American journal of pathology2017
M1 Macrophage-Induced Endothelial-to-Mesenchymal Transition Promotes Infantile Hemangioma Regression.
Article in The American journal of pathology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 41 citations in OpenAlex.
- Research Progress on Angiogenesis and Involution Mechanisms of Infantile Hemangioma and Its Regulation by Active Components ofInternational journal of molecular sciences · 2026Review
- SNAI2/SLUG: a key regulator of endothelial-to-mesenchymal transition and vascular remodeling in cardiovascular diseases.Journal of cardiothoracic surgery · 2026Review
- Determinants of proliferation and involution in infantile hemangioma: macrophage crosstalk, endothelial plasticity, and metabolic rewiring.Frontiers in pediatrics · 2026Review
- Immune microenvironment of infantile hemangioma: cellular dynamics, molecular networks, and emerging immunomodulatory strategies.Frontiers in immunology · 2026Review
- Causal effects of inflammatory cytokines on hemangioma mediated by blood metabolites: A two-step Mendelian randomization study.Journal of medical biochemistry · 2025Article
- Macrophage Ferroptotic Resistance Is Required for the Progression of Infantile Hemangioma.Journal of the American Heart Association · 2025Article
- Decoding infantile hemangioma: cellular dynamics, molecular signals, and microenvironmental influences.Frontiers in oncology · 2025Review
- Clinicopathological features and genetic mutation spectrum of primary anastomosing hemangioma arising from the kidney.Frontiers in immunology · 2025Article
- Advances in regulating endothelial-mesenchymal transformation through exosomes.Stem cell research & therapy · 2024Review
- Immunologic landscape of human hepatic hemangiomas and epithelioid hemangioendotheliomas.Hepatology communications · 2024Article
- Fucoidan and topography modification improvedBioactive materials · 2023Article
- M2 Macrophage-Derived Exosomal lncRNA MIR4435-2HG Promotes Progression of Infantile Hemangiomas by Targeting HNRNPA1.International journal of nanomedicine · 2023Article
- Targeting RUNX1 as a novel treatment modality for pulmonary arterial hypertension.Cardiovascular research · 2022Article
- Digital Staging of Hepatic Hemangiomas Reveals Spatial Heterogeneity in Endothelial Cell Composition and Vascular Senescence.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2022Article
- Inhibition of Bruton's Tyrosine Kinase Alleviates Monocrotaline-Induced Pulmonary Arterial Hypertension by Modulating Macrophage Polarization.Oxidative medicine and cellular longevity · 2022Article
- Notch pathway inhibitor DAPT acceleratesOncology letters · 2021Article
- Recent Advances in Understandings Towards Pathogenesis and Treatment for Intrauterine Adhesion and Disruptive Insights from Single-Cell Analysis.Reproductive sciences (Thousand Oaks, Calif.) · 2021Review
- Insights into Macrophage/Monocyte-Endothelial Cell Crosstalk in the Liver: A Role for Trem-2.Journal of clinical medicine · 2021Review
- Dysfunctional Vascular Endothelium as a Driver of Atherosclerosis: Emerging Insights Into Pathogenesis and Treatment.Frontiers in pharmacology · 2021Review
- Endothelial autophagy deficiency induces IL6 - dependent endothelial mesenchymal transition and organ fibrosis.Autophagy · 2020Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Infantile hemangiomas are benign tumors of vascular endothelial cells (ECs), characterized by three distinct stages: proliferating phase, involuting phase, and involuted phase. The mechanisms that trigger involution of hemangioma into fibro-fatty tissue remain unknown. We report a novel mechanism by which M1-polarized macrophages induce endothelial-to-mesenchymal transition (EndMT) and promote hemangioma regression. M1- but not M2-polarized macrophages induced EndMT in ECs. Tumor necrosis factor-α and, to a lesser extent, IL-1β and interferon-γ were the most potent cytokines produced by the M1 macrophages that induce in vitro EndMT. Western blot analysis and gene expression profiling showed that ECs treated with M1 macrophages, tumor necrosis factor-α, or IL-1β decreased the expression of endothelial markers, whereas mesenchymal markers increased concomitantly. Immunohistochemical staining of patient samples revealed that a significant perivascular infiltration of M1, but not M2, macrophages coincides with endothelial expression of the critical EndMT transcription factors Snail/Slug in involuting hemangiomas. Most strikingly, M1 macrophage-treated ECs isolated from patient hemangiomas (HemECs) but not untreated HemECs readily differentiated into adipocytes on adipogenic induction. Thus, in vitro EndMT and adipogenesis of HemECs have, in part, recapitulated the natural history of hemangioma regression. In conclusion, our findings indicate that EndMT induced by M1 macrophages promotes infantile hemangioma regression and may lead to novel therapeutic treatments for this vascular tumor.
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