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- W2740135538 abstract "Background: Endothelial dysfunction plays a critical role in the onset and progression of diabetic vascular complications. We have recently shown that hyperglycaemia-mediated dysregulation of TXNIP, an exquisitely glucose-inducible gene, induces widespread impairment in endothelial cell function and survival. We therefore hypothesised that dysregulation of TXNIP plays a causal role in diabetes-mediated endothelial dysfunction Methods and Results: To investigate the role of TXNIP in diabetes-mediated endothelial dysfunction, we generated an endothelial-specific TXNIP knockout (TXNIP-EKO) mouse model by crossing floxed TXNIP and VEcadherin-Cre mice. Diabetes were induced in 12-week old TXNIP-EKO male mice and floxed control wild type littermate (WTf) by intraperitoneal injection of streptozotocin. Aortic ring segments isolated from non-diabetic and diabetic TXNIP-EKO and WTf mice were pre-contracted with norepinephrine and assessed for acetylcholine-induced vasorelaxation ex vivo. In non-diabetic mice, segments from TXNIP-EKO mice displayed a greater relaxation compared to WTf mice in response to acetylcholine. Diabetes impaired vasorelaxation in WTf mice. Remarkably, diabetes-induced impairment in vasorelaxation was attenuated in TXNIP-EKO mice. Inhibition of nitric oxide synthase with L-NAME abolished acetylcholine-induced vasorelaxation in non-diabetic and diabetic WTf and TXNIP-EKO mice, indicating a nitric oxide-dependent relaxation. Endothelial-independent vasorelaxation induced by nitric oxide donor, sodium nitroprusside, was comparable between TXNIP-EKO and WTf mice. Conclusion: Endothelial-specific deletion of TXNIP is protective against diabetes-impaired endothelial dysfunction. These findings identify TXNIP is a novel target for treatment of diabetic vascular complications." @default.
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- W2740135538 date "2017-01-01" @default.
- W2740135538 modified "2023-10-17" @default.
- W2740135538 title "A Critical Role for Thioredoxin Interacting Protein (TXNIP) in Diabetes-Induced Endothelial Dysfunction" @default.
- W2740135538 doi "https://doi.org/10.1016/j.hlc.2017.06.158" @default.
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