Summary
Heart failure (HF) with preserved ejection fraction (HFpEF) is a prevalent disorder; however, our treatment options are limited. Studies show that endothelial cell (EC) dysfunction precedes the development of HFpEF and is a key player in the pathogenesis of this disorder. Hexokinases (HK) catalyze glucose phosphorylation, and one HK isoform (HK1) binds to the outer mitochondrial membrane via its N-terminal hydrophobic domain, encoded in its exon 1. We have generated a mouse model with deletion of the mitochondrial binding domain (MBD) of HK1 (designated as ΔE1HK1 herein). These mice display HF
