ArticleCell death & disease2020
Fruquintinib inhibits VEGF/VEGFR2 axis of choroidal endothelial cells and M1-type macrophages to protect against mouse laser-induced choroidal neovascularization.
Article in Cell death & disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.
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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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
17 citing papers in PubMed, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.
- Clinical research progress of fruquintinib in the treatment of malignant tumors.Investigational new drugs · 2024Pooled it
- Fruquintinib: Mechanism of Action, Clinical, and Translational Science.Clinical and translational science · 2026Review
- An Inhibitory Aptamer Against PDGF-C Overcomes Anti-VEGF Refractoriness and Reduces Choroidal Neovascularization and Fibrosis.Investigative ophthalmology & visual science · 2026Article
- Advances in the molecular signaling mechanisms of VEGF/VEGFR2 in fundus neovascularization disease (Review).Experimental and therapeutic medicine · 2025Review
- Clinical Progress of Fruquintinib in Colorectal Cancer: An Overview.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Light-Activated Anti-Vascular Combination Therapy against Choroidal Neovascularization.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Light-responsive polymeric nanoparticles for retinal drug delivery: design cues, challenges and future perspectives.Heliyon · 2024Review
- Non-Coding RNAs: Novel Regulators of Macrophage Homeostasis in Ocular Vascular Diseases.Biomolecules · 2024Review
- VEGFR-3 signaling in macrophages: friend or foe in disease?Frontiers in immunology · 2024Review
- Article
- Macrophage/microglia polarization for the treatment of diabetic retinopathy.Frontiers in endocrinology · 2023Review
- The cross-talk between macrophages and tumor cells as a target for cancer treatment.Frontiers in oncology · 2023Review
- The N6-Methyladenosine RegulatorInternational journal of molecular sciences · 2022Article
- PGECell communication and signaling : CCS · 2022Article
- Ocular Nanomedicine.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Review
- The Key Network of mRNAs and miRNAs Regulated by HIF1A in Hypoxic Hepatocellular Carcinoma Cells.Frontiers in genetics · 2022Article
- Identification of Diagnostic Biomarkers and Their Correlation with Immune Infiltration in Age-Related Macular Degeneration.Diagnostics (Basel, Switzerland) · 2021Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Wet age-related macular degeneration, which is characterized by choroidal neovascularization (CNV) and induces obvious vision loss. Vascular endothelial growth factor (VEGF) family member VEGF-A (also named as VEGF) and its receptor VEGFR2 contribute to the pathogenesis of CNV. Choroidal endothelial cells (CECs) secret C-C motif chemokine ligand 2 (CCL2), which attracts macrophages to CNV lesion and promotes macrophage M1 polarization. Accordingly, infiltrating macrophages secret inflammatory cytokines to promote CNV. In vivo, intravitreal injection of fruquintinib (HMPL-013), an antitumor neovascularization drug, alleviated mouse CNV formation without obvious ocular toxicity. Meanwhile, HMPL-013 inhibited VEGF/VEGFR2 binding in CECs and macrophages, as well as macrophage M1 polarization. In vitro, noncontact coculture of human choroidal vascular endothelial cells (HCVECs) and macrophages under hypoxia conditions was established. HMPL-013 downregulated VEGF/VEGFR2/phosphoinositide-3-kinase/protein kinase B (AKT)/nuclear factor kappa B pathway and CCL2 secretion in HCVECs, as well as VEGF/VEGFR2-induced macrophage M1 polarization under hypoxia condition. In addition, HMPL-013 inhibited HCEVC derived CCL2-induced macrophage migration and M1 polarization, along with macrophage M1 polarization-induced HCVECs proliferation, migration, and tube formation. Altogether, HMPL-013 alleviated CNV formation might via breaking detrimental cross talk between CECs and macrophages.
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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.