VEGF-B prevents chronic hyperglycemia-induced retinal vascular leakage by regulating the CDC42-ZO1/VE-cadherin pathway
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View abstract on PubMed
Summary
This summary is machine-generated.Vascular endothelial growth factor (VEGF)-B deficiency damages retinal vessels in early diabetic retinopathy (DR). Restoring VEGF-B prevents vascular leakage and may offer a novel therapy for DR.
Area Of Science
- Ophthalmology
- Diabetology
- Molecular Biology
Background
- Non-proliferative diabetic retinopathy (NPDR) is an early stage of diabetic retinopathy (DR), characterized by chronic oxidative stress and limited treatment options.
- Understanding the mechanisms of diabetic retinal micro-vasculopathy is crucial for developing early interventions.
Purpose Of The Study
- To investigate the pathogenic mechanisms of diabetes-induced retinal micro-vasculopathy.
- To explore vascular endothelial growth factor (VEGF)-B as a potential therapeutic target for early DR.
Main Methods
- Established a type 1 diabetes mouse model using streptozotocin (STZ).
- Analyzed retinal tissues using label-free quantitative proteomics and bioinformatics.
- Investigated VEGF-B's role in human retinal vascular endothelial cells (HRECs) via knockdown and overexpression.
- Assessed therapeutic effects of VEGF-B on vascular leakage in vitro and in vivo.
Main Results
- Reduced expression of VEGF-B and CDC42 observed in early DR retinal tissues.
- VEGF-B upregulated CDC42/ZO1/VE-cadherin, preventing hyperglycemia-induced vascular leakage in HRECs.
- Intravitreal VEGF-B injections improved retinal vascular leakage and neurovascular response in DR mice.
Conclusions
- Decreased VEGF-B expression leads to retinal vessel damage in diabetes via downregulation of CDC42/ZO1/VE-cadherin.
- VEGF-B demonstrates therapeutic potential for treating early diabetic retinopathy.
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