Researchers are interested in provoking the body into growing additional blood vessels that can bypass areas of damage. Most of this work is focused on restoring long term supply of blood to heart tissue following a heart attack, and thus on regrowth in an environment of damage and damage-related signaling. It would be perhaps more interesting to develop means of growing additional redundant blood vessels prior to that point, in the normal signaling environment. This could greatly reduce the damage done by a blockage that would ordinarily cause a heart attack, and slow the progression into heart failure caused by narrowing of blood vessels. This all compares poorly to developing means of prevention of atherosclerosis, the cause of blood vessel narrowing, rupture, and blockage, but even given a cure for atherosclerosis, there is a lot to be said for having redundant routes of blood supply to major organs.
Cardiovascular disease is the leading cause of mortality and ischemic heart disease is a major cause of death worldwide. Coronary vessels that nourish the heart develop from three main sources, the endocardium on the inner surface of the hearts blood-filled chambers being one of the major contributors. In normal conditions, the adult heart can no longer generate new blood vessels from the endocardium, because the endocardium-to-coronary vessel transition is blocked by a connective tissue wall beneath the endocardium.
In a recently published study researchers show that the VEGF-B growth factor can be used to activate the growth of vessels inside of the heart during cardiac ischemic damage. This novel finding opens the possibility that vessels emerging from the inner side of the heart could be further developed for the treatment of myocardial infarction, which results from insufficient delivery of oxygen to cardiac tissue. In normal conditions, blood nourishes the adult heart through coronary vessels.
VEGF-B (vascular endothelial growth factor) belongs to a family of growth factors that regulate the formation of blood- and lymphatic vessels. Earlier attempts to utilize another growth factor gene, VEGF-A, to grow new vessels in the heart have failed, mostly due to the leakiness of the vessels and increased inflammation caused by VEGF-A, but not by VEGF-B. Re-activation of the embryonic vessel growth program in adult endocardium could be a new therapeutic strategy for cardiac neovascularization after myocardial infarction. For possible future clinical use, the function of these vessels and their blood flow has to be further studied to ensure that they really increase transport of oxygen and nutrients into the cardiac muscle.