Related Experiment Video

Updated: May 12, 2025

Laser-Induced Chronic Ocular Hypertension Model on SD Rats
06:34

Laser-Induced Chronic Ocular Hypertension Model on SD Rats

Published on: December 4, 2007

11.3K

Glucagon-Like Peptide 1 Receptor Agonist Stimulation Inhibits Laser-Induced Choroidal Neovascularization by

Akira Machida1, Keiji Suzuki2, Takafumi Nakayama2

  • 1Department of Ophthalmology and Visual Sciences, Graduate School of Biomedical Sciences, Nagasaki University, Nagasaki, Nagasaki Prefecture, Japan.

Investigative Ophthalmology & Visual Science
|May 7, 2025
PubMed
Abstract

Insights

Glucagon-like peptide-1 receptor (GLP-1R) agonists, like liraglutide, effectively reduce choroidal neovascularization (CNV) by inhibiting the NLRP3 inflammasome. This suggests GLP-1R agonists may be a viable adjunctive therapy for exudative age-related macular degeneration (AMD).

Area of Science:

  • Ophthalmology
  • Endocrinology
  • Immunology

Background:

  • The glucagon-like peptide-1 receptor (GLP-1R) is a therapeutic target for diabetes with known neuroprotective and anti-inflammatory effects.
  • While GLP-1's role in diabetic and ischemic retinopathies is established, its impact on choroidal neovascularization (CNV) in exudative age-related macular degeneration (AMD) is not well understood.

Purpose of the Study:

  • To investigate the effects of GLP-1 on CNV in a laser-induced mouse model.
  • To determine if GLP-1R agonists can suppress CNV formation and explore the underlying mechanisms.

Main Methods:

  • Ex vivo sprouting assays were used to test the anti-angiogenic effects of GLP-1.
  • GLP-1R localization in laser-induced CNV lesions was analyzed using immunohistochemistry.
  • Liraglutide, a GLP-1R agonist, was administered subcutaneously or intravitreally, and CNV formation was assessed via RT-qPCR and histological analysis.

Main Results:

  • GLP-1R was detected in CNV lesions, co-localizing with activated microglia/macrophages, retinal pigment epithelial cells, and endothelial cells.
  • Liraglutide significantly inhibited angiogenesis in vitro and reduced CNV formation in vivo through both administration routes.
  • Liraglutide suppressed the expression of NLRP3 inflammasome components (NLRP3, IL-1β, IL-6, TNF).

Conclusions:

  • Liraglutide suppresses CNV formation, likely by inhibiting the NLRP3 inflammasome pathway.
  • Intraocular GLP-1R signaling appears to mediate these anti-CNV effects.
  • GLP-1R agonists represent a potential adjunctive therapy for exudative AMD, warranting further clinical investigation.

More Related Videos

A Mouse Model for Laser-induced Choroidal Neovascularization07:08

A Mouse Model for Laser-induced Choroidal Neovascularization

Published on: December 27, 2015

17.5K
In Vivo Multimodal Imaging and Analysis of Mouse Laser-Induced Choroidal Neovascularization Model09:56

In Vivo Multimodal Imaging and Analysis of Mouse Laser-Induced Choroidal Neovascularization Model

Published on: January 21, 2018

9.0K

Related Concept Videos

Open Angle Glaucoma: Treatment01:27

Open Angle Glaucoma: Treatment

In open-angle glaucoma, the iridocorneal angle remains open, but the trabecular meshwork becomes stiff, slowing down the outflow of aqueous humor. This causes a buildup of aqueous humor in the anterior chamber, leading to a sudden increase in intraocular pressure. The treatment for open-angle glaucoma focuses on reducing the elevated intraocular pressure by either decreasing the secretion of aqueous humor or increasing its outflow.
Drugs such as carbonic anhydrase inhibitors, α2- and...
362
Glucagon-like Receptor Agonists01:24

Glucagon-like Receptor Agonists

Incretins include glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), which stimulate insulin secretion post-meals. In type 2 diabetes, GIP's efficacy is reduced, making GLP-1 a viable drug target. GIP originates from preproGIP.
GLP-1, when administered in high doses intravenously, triggers insulin secretion, inhibits glucagon release, slows gastric emptying, reduces food intake, and restores normal insulin secretion. However, its rapid inactivation by...
266
Angle Closure Glaucoma: Treatment01:28

Angle Closure Glaucoma: Treatment

Angle-closure glaucoma, or closed-angle glaucoma, is an eye condition where the iris bulges out and blocks the iridocorneal angle, resulting in a buildup of aqueous humor and increased intraocular pressure. Immediate medical attention is necessary due to the sudden onset of symptoms. The treatment for angle-closure glaucoma includes short-term and long-term approaches. Short-term treatment involves using eye drops like pilocarpine to lower intraocular pressure by increasing aqueous humor...
385
Glaucoma: Overview01:25

Glaucoma: Overview

Glaucoma is an eye condition characterized by increased intraocular pressure that damages the retina and optic nerve, leading to irreversible blindness if left untreated. The human eye has various components, including the cornea, iris, pupil, lens, and optic nerve. Aqueous humor is secreted by the epithelium of the ciliary body in the posterior chamber and flows through the trabecular meshwork and canal of Schlemm, maintaining normal intraocular pressure. The trabecular meshwork and the canal...
478