ArticleInvestigative ophthalmology & visual science2021
VEGFR2 Trafficking by KIF13B Is a Novel Therapeutic Target for Wet Age-Related Macular Degeneration.
Article in Investigative ophthalmology & visual science, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 30 citations in OpenAlex.
- Eye Drop Development of Anti-VEGF Therapeutics by Ocular Penetrating Carrier to the Posterior Region of the Eye.Translational vision science & technology · 2026Article
- Vascular smooth muscle cell-derived KIF13B inhibits proinflammatory responses to protect against atherosclerosis.The Journal of clinical investigation · 2026Article
- Protein Kinase D Regulates Kinesin-Mediated VEGFR2 Trafficking and Influences Retinal Endothelial Permeability.Traffic (Copenhagen, Denmark) · 2026Article
- A mutation inMolecular vision · 2026Article
- Macrophage-derived KIF13B interacts with USP9X to attenuate abdominal aortic aneurysm development by potentiating TFEB stability.Theranostics · 2025Article
- Treatment of neovascular age-related macular degeneration with anti-vascular endothelial growth factor drugs: progress from mechanisms to clinical applications.Frontiers in medicine · 2024Review
- Review
- CM082 suppresses hypoxia-induced retinal neovascularization in larval zebrafish.Frontiers in pharmacology · 2024Article
- Peptide-Based Agents for Cancer Treatment: Current Applications and Future Directions.International journal of molecular sciences · 2023Review
- Review
- KIF13B mediates VEGFR2 recycling to modulate vascular permeability.Cellular and molecular life sciences : CMLS · 2023Article
- Rethinking the potential and necessity of drug delivery systems in neovascular age-related macular degeneration therapy.Frontiers in bioengineering and biotechnology · 2023Review
- A novel approach in preventing vascular leakage and angiogenesis in wet age-related macular degeneration.Neural regeneration research · 2022Article
- Application and mechanism of anti-VEGF drugs in age-related macular degeneration.Frontiers in bioengineering and biotechnology · 2022Review
- KIF13B-mediated VEGFR2 trafficking is essential for vascular leakage and metastasis in vivo.Life science alliance · 2022Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Purpose: Vascular endothelial growth factor (VEGF) and its receptor VEGFR2 are promising therapeutic targets for wet age-related macular degeneration (AMD). As a topically applicable option, we developed the peptide KAI to selectively interfere with VEGFR2 trafficking to the cell surface where it receives VEGF. This study sought to determine the efficacy of KAI in the mouse model of choroidal neovascularization (CNV). Methods: The specificity of KAI was tested by surface plasmon resonance. The drug delivery was analyzed by cryosection and the ELISA after treatment of KAI eyedrop to the mouse eyes. For the laser-induced CNV model, mice with laser-induced ruptures in Bruch's membrane received daily treatment of KAI eyedrop or control peptide. The other groups of mice received intravitreal injection of anti-VEGF or IgG control. After two weeks, CNV was quantified and compared. Results: First, we showed the specificity and high affinity of KAI to VEGFR2. Next, biodistribution revealed successful delivery of KAI eyedrop to the back of the mouse eyes. KAI significantly reduced the disease progression in laser-induced CNV. The comparison with current therapy suggests that KAI eyedrop is as effective as current therapy to prevent CNV in wet AMD. Moreover, the genetic deletion of a kinesin KIF13B, which mediates VEGFR2 trafficking to the cell surface, confirmed the pivotal role of KIF13B in disease progression of wet AMD and neovascularization from choroidal vessels. Conclusions: Taken together, pharmacologic inhibition and genetic deletion complementarily suggest the therapeutic possibility of targeting VEGFR2 trafficking to inhibit pathological angiogenesis in wet AMD.
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