PRKG1 and endothelial dysfunction: Based on our previous findings illustrating that impaired NO bioavailability, a hallmark of endothelial dysfunction (13, 36, 37), could be increased by i.v. application of placenta-derived stromal cells (11), we suggested that the improved diastolic performance following WT and CD362− MSC administration (25) was caused by changes of the NO-cGMP-PKG pathway.