ArticleJournal of neuroinflammation2020
Macrophage to myofibroblast transition contributes to subretinal fibrosis secondary to neovascular age-related macular degeneration.
Article in Journal of neuroinflammation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 papers.
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Who cites it
89 citing papers in PubMed.
- Effects of vascular endothelial growth factor and angiopoietin-2 inhibitions on intraretinal hyperreflective foci in neovascular age-related macular degeneration.Japanese journal of ophthalmology · 2026Article
- Complement Activation by Post-Translationally Modified Proteins: Links to Chronic Inflammation and Autoimmunity.Immunological reviews · 2026Review
- A Novel Ocular Fibrosis Signature for AMD Using the Two-Stage Laser-Induced Subretinal Fibrosis Mouse Model.Investigative ophthalmology & visual science · 2026Article
- Nicotinamide Mononucleotide Attenuates Inflammatory Activation, Choroidal Neovascularization, and Lesion-Associated Remodeling.Investigative ophthalmology & visual science · 2026Article
- Macrophage-to-myofibroblast transition-derived itaconate promotes bone metastasis in lung cancer through targeting of HSPA8.Experimental & molecular medicine · 2026Article
- Macrophage-to-Myofibroblast Transdifferentiation Contributes to Pulmonary Fibrosis via the MERTK-SPP1-SRC-TKS5 Signaling Axis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Piezo1 promote macrophage-to-myofibroblast transition and bladder fibrosis in neurogenic bladder.World journal of urology · 2026Article
- Complement C5a Promotes Epithelial-Mesenchymal Transition in Pterygium via C5aR Activation.Investigative ophthalmology & visual science · 2026Article
- Association Between PCSK9 Inhibitor Use and Risk of Age-Related Macular Degeneration.Translational vision science & technology · 2026Article
- TNFAIP3 in M2 Macrophage Attenuates Subretinal Fibrosis in Laser-Induced Murine Model.Investigative ophthalmology & visual science · 2026Article
- Macrophage-to-myofibroblast transition (MMT) - An adverse response to polypropylene mesh implanted for pelvic organ prolapse repair surgery in a non-human primate model.Biomaterials · 2026Article
- RPE With ROCK-Mediated Epithelial-Mesenchymal Transition as a Key Contributor of Subretinal Fibrosis in AMD.Investigative ophthalmology & visual science · 2026Article
- MSC-EVs attenuate subretinal fibrosis in choroidal neovascularization through miR-21-5p-mediated inhibition of EMT and MMT and suppression of inflammation.Journal of neuroinflammation · 2026Article
- A sequential dual-drug delivery system for multi-target inhibition of subretinal fibrosis.Journal of nanobiotechnology · 2026Article
- Myofibroblast lineage mapping and inhibiting subretinal fibrosis by targeting SMAD3 and MRTF pathways via microRNA-24 functional study.bioRxiv : the preprint server for biology · 2026Article
- The Role of the C3a-C3aR Pathway in Diseases: Latest Research Advances.Mediators of inflammation · 2026Review
- Dapagliflozin attenuates diabetic renal fibrosis by inhibiting macrophage-myofibroblast transitionPeerJ · 2026Article
- Cathepsin H drives hypoxia-associated inflammatory and angiogenic programs in diabetic retinopathy and represents a potential therapeutic target.International journal of biological sciences · 2026Article
- The authors respond to feedback onFrontiers in oncology · 2026Article
- Targeting Macrophage-to-Myofibroblast Transition Mitigates Progression from Inflammation to Fibrosis in Rosacea.International journal of biological sciences · 2026Article
29 more citing papers are in PubMed but not listed here.
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Authors and funding
7 authors.
Funding
Abstract
backgroundMacular fibrosis causes irreparable vision loss in neovascular age-related macular degeneration (nAMD) even with anti-vascular endothelial growth factor (VEGF) therapy. Inflammation is known to play an important role in macular fibrosis although the underlying mechanism remains poorly defined. The aim of this study was to understand how infiltrating macrophages and complement proteins may contribute to macular fibrosis.
methodsSubretinal fibrosis was induced in C57BL/6J mice using the two-stage laser protocol developed by our group. The eyes were collected at 10, 20, 30 and 40 days after the second laser and processed for immunohistochemistry for infiltrating macrophages (F4/80 and Iba-1), complement components (C3a and C3aR) and fibrovascular lesions (collagen-1, Isolectin B4 and α-SMA). Human retinal sections with macular fibrosis were also used in the study. Bone marrow-derived macrophages (BMDMs) from C57BL/6J mice were treated with recombinant C3a, C5a or TGF-β for 48 and 96 h. qPCR, Western blot and immunohistochemistry were used to examine the expression of myofibroblast markers. The involvement of C3a-C3aR pathway in macrophage to myofibroblast transition (MMT) and subretinal fibrosis was further investigated using a C3aR antagonist (C3aRA) and a C3a blocking antibody in vitro and in vivo.
resultsApproximately 20~30% of F4/80
conclusionsMMT plays a role in macular fibrosis secondary to nAMD. MMT can be induced by TGF-β and C3a but not C5a. Further research is required to fully understand the role of MMT in macular fibrosis. Macrophage to myofibroblast transition (MMT) contributes to subretinal fibrosis. Subretinal fibrosis lesions contain various cell types, including macrophages and myofibroblasts, and are fibrovascular. Myofibroblasts are key cells driving pathogenic fibrosis, and they do so by producing excessive amount of extracellular matrix proteins. We have found that infiltrating macrophages can transdifferentiate into myofibroblasts, a phenomenon termed macrophage to myofibroblast transition (MMT) in macular fibrosis. In addition to TGF-β1, C3a generated during complement activation in CNV can also induce MMT contributing to macular fibrosis. RPE = retinal pigment epithelium. BM = Bruch's membrane. MMT = macrophage to myofibroblast transition. TGFB = transforming growth factor β. a-SMA = alpha smooth muscle actin. C3a = complement C3a.
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