2. Academic Validation
  3. Involvement of Lgals3/Galectin-3 in Choroidal Neovascularization and Subretinal Fibrosis Formation

Involvement of Lgals3/Galectin-3 in Choroidal Neovascularization and Subretinal Fibrosis Formation

  • Biomedicines. 2024 Nov 20;12(11):2649. doi: 10.3390/biomedicines12112649.
Di Wu 1,  Ye Liu 1,  Xiaogang Luo 1,  Zhiqing Chen 1,  Qiuli Fu 1,  Ke Yao 1
Affiliations

Affiliation

  • 1 Eye Center, The Second Affiliated Hospital, School of Medicine, Zhejiang University, Zhejiang Provincial Key Laboratory of Ophthalmology, Zhejiang Provincial Clinical Research Center for Eye Diseases, Zhejiang Provincial Engineering Institute on Eye Diseases, Hangzhou 310051, China.
PMID: 39595213 DOI: 10.3390/biomedicines12112649
Abstract

Background:Lgals3/Galectin-3 plays a pivotal role in many vascular diseases. However, the involvement of Lgals3/Galectin-3 in eyes with neovascular age-related macular degeneration (nAMD) remains unknown. Methods: In the laser-induced CNV model, a whole mount retina stained with Isolectin B4 and collagen type I revealed the vascular bed and CNV-associated subretinal fibrosis on day 7 after laser treatment. Results: We show that the expression levels of Lgals3/Galectin-3 were significantly increased in the RPE/choroidal complex of CNV mice. An intravitreal injection of Lgals3-siRNA significantly suppressed the area of CNV and subretinal fibrosis, together with Mcp-1 decline. The mixture of Lgals3-siRNA and Ranibizumab showed more efficiency than each drug used separately. Hypoxia induced Lgals3/Galectin-3 production in ARPE-19 cells, which was reduced by the silencing hypoxia-inducible factor -1α (Hif-1a). Conclusions: Our data indicated that Lgals3/Galectin-3 is involved in the pathogenesis of CNV and subretinal fibrosis, and Lgals3/Galectin-3 could be a potential therapeutic target for nAMD.

Keywords

Lgals3/galectin-3; age-related macular degeneration; choroidal neovascularization; hypoxia-inducible factor; subretinal fibrosis.

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