ArticleInflammation2022
Crosstalk Between RPE Cells and Choroidal Endothelial Cells via the ANXA1/FPR2/SHP2/NLRP3 Inflammasome/Pyroptosis Axis Promotes Choroidal Neovascularization.
Article in Inflammation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 20 citations in OpenAlex.
- Annexin A1 as a Key Modulator of Inflammatory, Glial, and Angiogenic Signaling Pathways in Diabetic Retinopathy.Investigative ophthalmology & visual science · 2026Article
- Effects of New P2X7R Antagonists on Retinal Inflammatory Degenerative Conditions.Inflammation · 2026Article
- Irigenin Modulates BL-Induced Pyroptosis in Retinal Pigment Epithelial Cells Through p38 MAPK and NFκB Pathways.Journal of biochemical and molecular toxicology · 2026Article
- Hypoxia induced DNMT3B and SHP2 signaling promoted HCC via suppressing P53 and MYH11 protein expression.Frontiers in oncology · 2026Article
- The role of NLRP3 inflammasome in age-related macular degeneration: mechanisms and therapeutic prospects.Frontiers in aging neuroscience · 2026Review
- Early proteomic and metabolomic signatures in diabetes associated with progression to diabetic retinopathy over 1-2 years.Frontiers in endocrinology · 2026Article
- Pharmacovigilance analysis of vision disorders relating to brimonidine treatment and mechanism study using network toxicology and molecular docking.Scientific reports · 2025Article
- Exploring the therapeutic potential of annexin A1-derived peptide AcMolecular and cellular biochemistry · 2025Article
- Endoplasmic reticulum-mitochondria coupling prompts ZBP1-mediated RPE cell PANoptosis in age-related macular degeneration.Communications biology · 2025Article
- DUSP1 alleviates LPS-induced acute lung injury by inhibiting the SHP2-JNK axis and mitochondrial apoptosis.American journal of translational research · 2025Article
- ω-3PUFAs Inhibit Hypoxia-Induced Retinal Neovascularization via Regulating Microglial Pyroptosis through METTL14-Mediated m6A Modification of IFNB1 mRNA.Applied biochemistry and biotechnology · 2024Article
- Lack of Annexin A1 Exacerbates Inflammatory Response in Acute Endometritis Model.Inflammation · 2024Article
- Annexin A1 in the nervous and ocular systems.Neural regeneration research · 2024Review
- Exploring the Role of ROCK Inhibition in Corneal Edema Through Crosstalk Between Epithelial and Endothelial Cells.Journal of ophthalmology · 2024Review
- A simplified protocol to induce hypoxia in a standard incubator: A focus on retinal cells.Experimental eye research · 2023Article
- Research Progress of Bioinspired Nanostructured Systems for the Treatment of Ocular Disorders.Pharmaceuticals (Basel, Switzerland) · 2023Review
- Resolution of Inflammation in Retinal Disorders: Briefly the State.International journal of molecular sciences · 2022Review
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
One type of age-related macular degeneration (AMD), neovascular (nAMD), characterized by choroidal neovascularization (CNV), accounts for the majority of the severe central vision impairment associated with AMD. Endothelial cells (ECs) in direct contact with retinal pigment epithelial (RPE) cells are more prone to the pathological angiogenesis involved in CNV. Herein, we investigated the effect of crosstalk between RPE cells and choroidal endothelial cells (CECs) via the ANXA1/FPR2/NLRP3 inflammasome/pyroptosis axis on the development of choroidal neovascularization (CNV) in vitro and in vivo. ANXA1 expression and secretion from ARPE-19 cells were upregulated by hypoxia. FPR2 expression, especially on the plasma membrane, in HCECs was upregulated under hypoxic conditions. ANXA1 secreted from ARPE-19 cells inhibited NLRP3 inflammasome activation and NLRP3 inflammasome-mediated pyroptosis in HCECs by activating the FPR2/SHP2 axis. Moreover, ANXA1 secreted by ARPE-19 cells promoted behaviors of HCECs, including proliferation, migration, and tube formation, by activating the FPR2/SHP2 axis and inhibiting NLRP3 inflammasome-mediated pyroptosis. Inhibiting the upregulated ANXA1/FPR2/SHP2/NLRP3 inflammasome/pyroptosis axis decreased the volume of CNV. Our data suggest that the crosstalk between RPE cells and CECs via the ANXA1/FPR2/NLRP3 inflammasome/pyroptosis axis promotes CNV. This finding could identify a potential target for the prevention and treatment of CNV.
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