Therefore, the aims of this investigation were as follows: first, to verify that vascular endothelial dysfunction is caused by a decrease in NO bioavailability in hypercholesterolemia, and on this basis, to observe and analyze whether MPO directs endothelial dysfunction in hypercholesterolemia by affecting the vascular NO/cGMP/cGK signaling pathway. Here, PRKG1 is linked to familial hypercholesterolemia.