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Endothelial glycocalyx is damaged in diabetic cardiomyopathy: angiopoietin 1 restores glycocalyx and improves diastolic function in mice – published online 25/02/2022

Qiu graphical abstract

Yan Qiu, Stanley Buffonge, Raina Ramnath, Sophie Jenner, Sarah Fawaz, Kenton P. Arkill, Chris Neal, Paul Verkade, Stephen J. White, Melanie Hezzell, Andrew H. J. Salmon, M.-Saadeh Suleiman, Gavin I. Welsh, Rebecca R. Foster, Paolo Madeddu, Simon C. Satchell

Diabetic cardiomyopathy is a serious and under-recognised complication of diabetes. The first sign is diastolic dysfunction, which progresses to heart failure. Endothelial glycocalyx plays multiple vital roles in the microcirculation and whilst it is known to be compromised in diabetes, it has not previously been studied in the coronary microcirculation in diabetes. In this issue, Qiu et al ( report that, in mouse models of diabetes, diastolic dysfunction is associated with glycocalyx loss from coronary microvascular endothelial cells and increased microvascular permeability. The authors also show that endothelial glycocalyx damage is sufficient to impair cardiac function. They provide evidence for increased matrix metalloproteinase activity as a potential mechanism of endothelial glycocalyx damage. They go on to demonstrate that angiopoietin 1 restores the endothelial glycocalyx and ameliorates diastolic dysfunction in diabetes. The authors conclude that these findings identify coronary microvascular endothelial glycocalyx damage as a contributor to the development of diabetic cardiomyopathy and, therefore, as a therapeutic target for heart failure in people with diabetes.

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