An advanced endothelial murine HFpEF model: eNOS is critical for angiotensin 1 –7 rescue of the diabetic phenotype

Diabetes and obesity are hallmark clinical features of patients with heart failure with preserved ejection fraction (HFpEF). [1,2] Activation of the renin-angiotensin system (RAS) can exacerbate HFpEF and is a primary cause of cardiorenal and vascular injury in patients living with different forms of metabolic syndrome. [1,2] Heightened Ang II signaling drives cardiorenal maladaptation in diabetic pathological states. [1,3,4] Angiotensin-converting enzyme 2 (ACE2) metabolizes Ang II into Ang 1 –7, offering an endogenous counterregulatory RAS axis which is frequently dysregulated in diseased states.
Source: Journal of Molecular and Cellular Cardiology - Category: Cytology Authors: Tags: Letter to the editor Source Type: research