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Sodium glucose transporter 2 inhibition reduces arterial stiffness and improves endothelial function in a mouse model of aging
Aging of the vasculature is characterized by arterial stiffening and endothelial dysfunction, both key events in the pathogenesis of cardiovascular disease (CVD). Thus, novel strategies are urgently needed to prevent and ameliorate vascular aging. In this context, treatment with sodium glucose trans...
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Published in: | The FASEB journal 2021-05, Vol.35 (S1), p.n/a, Article fasebj.2021.35.S1.02530 |
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Main Authors: | , , , , , , |
Format: | Article |
Language: | English |
Online Access: | Get full text |
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Summary: | Aging of the vasculature is characterized by arterial stiffening and endothelial dysfunction, both key events in the pathogenesis of cardiovascular disease (CVD). Thus, novel strategies are urgently needed to prevent and ameliorate vascular aging. In this context, treatment with sodium glucose transporter 2 inhibitors (SGLT2i) is now known to decrease cardiovascular morbidity and mortality in subjects with type 2 diabetes, heart failure, and chronic kidney disease. However, whether SGLT2i attenuates aging‐related arterial stiffening and endothelial dysfunction, thereby reducing CVD risk is unknown. Herein, we tested the hypothesis that treatment with SGLT2i (Empagliflozin) reduces arterial stiffness and endothelial dysfunction in aging. To test this hypothesis, we assessed aortic stiffness (in vivo via pulse‐wave velocity and ex vivo via atomic force microscopy) and mesenteric artery stiffness and endothelial function (via pressure myography mechanical responses and flow‐mediated dilation, respectively) in Empagliflozin ‐treated (14 mg/kg/day for 6 weeks) and control (standard chow diet) 80 week‐old C57BL/6J male mice (n=9 per group). We report that the Empagliflozin ‐treated cohort exhibited reduced aortic and mesenteric artery stiffness (p |
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ISSN: | 0892-6638 1530-6860 |
DOI: | 10.1096/fasebj.2021.35.S1.02530 |