ArticleInternational journal of molecular sciences2025
The Role of the Mitogen-Activated Protein Kinase Pathway in the Development of Laser-Induced Choroidal Neovascularization.
Article in International journal of molecular sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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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Who cites it
1 citing paper in PubMed.
- Streamlined synthetic regulatory cassette for efficient and photoreceptor-enriched retinal gene expression.Molecular therapy. Nucleic acids · 2026Article
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Authors and funding
12 authors.
Funding
Abstract
The role of the mitogen-activated protein kinase (MAPK) pathway in choroidal neovascularization (CNV) remains unclear. This study investigates the involvement of extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK), and p38 pathways in CNV development, as well as the therapeutic potential of sprouty 2 (SPRY2), an MAPK inhibitor, in a laser-induced mouse model. The expressions of ERK, JNK, and p38 proteins were analyzed using Western blotting and immunostaining. Immunofluorescence imaging revealed increased p-ERK and p-JNK expression in the retina, retinal pigment epithelium (RPE), and choroid up to day 7. Co-immunostaining showed p-ERK colocalized with CD31, CD11b, F4/80, cytokeratin, and GFAP in the retina, while p-JNK and p-p38 were associated with angiogenesis and inflammation throughout the retina and choroid. Compared to aflibercept, SPRY2 administration significantly inhibited CNV lesions, endothelial proliferation, fibrosis, and apoptosis, while better-preserving RPE integrity. SPRY2-treated mice showed a stronger reduction in CNV-related inflammation, epithelial-mesenchymal transition, and photoreceptor apoptosis. These results highlight the MAPK pathway's role in CNV pathogenesis, with ERK primarily mediating Müller cell gliosis and JNK, contributing to angiogenesis and inflammation. SPRY2 effectively suppressed CNV lesions, supporting its potential as a therapeutic target for CNV treatment via MAPK pathway modulation.
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