Drug therapies to inhibit Dkk1 function may limit arteriosclerotic disease, study finds

Targeting drug therapies at Dkk1 functioning could limit arteriosclerotic disease, researchers say

Drug therapies designed to inhibit endothelial Dkk1 signalling could help limit arteriosclerotic disease to prevent the thickening and hardening of the arteries.

Research published online by Arteriosclerosis, Thrombosis and Vascular Biology explained how the molecular and cellular pathway that leads to the hardening of the arteries involves a particularly damaging protein known as Dkk1.

Dr Dwight Towler, director of the cardiovascular pathobiology programme at Stanford-Burnham, said the next strategy would be to find ways to modulate Dkk1 function but in a time-sensitive and cell type-specific way.

He added: "In diseases such as chronic renal deficiency or diabetes, where unregulated Dkk1 signalling can be destructive, it may be appropriate to restrain the action of Dkk1 for a prolonged period of time."

Although Dkk1 is important for wound repair, inflammatory responses inside the artery walls after the onset of hyperglycemia, can trigger destructive Dkk1 signalling, the study explained.

It was further argued that drugs targeting this protein would been to focus on places where inhibition is called for, such as in the arteries in the case of arteriosclerotic disease, because healthy Dkk1 signalling regulates normal processes like joint remodelling.