Neuraminidase inhibition improves endothelial function in diabetic mice

Author:

Foote Christopher A.12,Ramirez-Perez Francisco I.1ORCID,Smith James A.13,Ghiarone Thaysa1,Morales-Quinones Mariana1ORCID,McMillan Neil J.13ORCID,Augenreich Marc A.13ORCID,Power Gavin13,Burr Katherine1,Aroor Annayya R.45,Bender Shawn B.56ORCID,Manrique-Acevedo Camila145ORCID,Padilla Jaume135ORCID,Martinez-Lemus Luis A.127ORCID

Affiliation:

1. NextGen Precision Health, University of Missouri, Columbia, Missouri, United States

2. Department of Medical Pharmacology and Physiology, University of Missouri, Columbia, Missouri, United States

3. Department of Nutrition and Exercise Physiology, University of Missouri, Columbia, Missouri, United States

4. Division of Endocrinology, Diabetes and Metabolism, Department of Medicine, University of Missouri, Columbia, Missouri, United States

5. Research Service, Harry S. Truman Memorial Veterans Hospital, Columbia, Missouri, United States

6. Department of Biomedical Sciences, University of Missouri, Columbia, Missouri, United States

7. Department of Medicine, Center for Precision Medicine, University of Missouri, Columbia, Missouri, United States

Abstract

This work identifies neuraminidase as a key mediator of endothelial dysfunction in type 2 diabetes that may serve as a biomarker for impaired endothelial function and predictive of development and progression of cardiovascular pathologies associated with type 2 diabetes (T2D). Data show that intervention with the neuraminidase inhibitor zanamivir at effective plasma concentrations may represent a novel pharmacological strategy for restoring the glycocalyx and ameliorating endothelial dysfunction.

Funder

HHS | NIH | NHLBI | NHLBI Division of Intramural Research

National Science Foundation

Publisher

American Physiological Society

Subject

Physiology (medical),Cardiology and Cardiovascular Medicine,Physiology

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