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Published on: June 15, 2018
Circular RNA RSU1 promotes retinal vascular dysfunction by regulating miR-345-3p/TAZ
Yiting Zhang1, Jianping Hu2,3, Xiaoying Qu4
1The First Affiliated Hospital of Chongqing Medical University, Chongqing Key Laboratory of Ophthalmology, Chongqing Eye Institute, and Chongqing Branch of National Clinical Research Center for Ocular Diseases, Chongqing, China.
Diabetic retinopathy causes vision loss. This study identifies circRSU1 as a key factor promoting vascular dysfunction in diabetic retinopathy by regulating TAZ levels, offering a potential therapeutic target.
Area of Science:
- Ophthalmology
- Molecular Biology
- Endocrinology
Background:
- Diabetic retinopathy is a leading cause of blindness.
- The molecular mechanisms of diabetic vascular complications are not fully understood.
- Circular RNAs (circRNAs) are implicated in vascular progression.
Purpose of the Study:
- To investigate the role of circRSU1 in diabetic retinopathy.
- To elucidate the underlying molecular mechanisms of circRSU1-mediated vascular dysfunction.
- To identify circRSU1 as a potential therapeutic target for diabetic vascular complications.
Main Methods:
- circRNA chip experiments identified circRSU1 overexpression in diabetic retinopathy patients.
- Human retinal endothelial cells were transfected with circRSU1 interference plasmids.
- Mechanistic studies involved assessing miR-345-3p sponging and TAZ levels.
Main Results:
- circRSU1 downregulation alleviated diabetic retinopathy-induced vascular dysfunction.
- Reduced circRSU1 led to decreased vascular endothelial growth factor, inflammation, and oxidative stress.
- circRSU1 upregulates TAZ by sponging miR-345-3p; TAZ downregulation reversed hyperglycemia-induced vascular dysfunction.
Conclusions:
- Overexpressed circRSU1 exacerbates diabetic vascular dysfunction by sponging miR-345-3p and increasing TAZ.
- circRSU1 represents a promising therapeutic target for managing diabetes mellitus-induced vascular complications.
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