Producing More Blood Vessels in Heart Tissue as a Way to Increase Resistance to the Damage of a Heart Attack
This is a fairly interesting take on reducing the impact of heart attacks. It isn't the best approach to the situation, which is to find methods of prevention, but rather a matter of engineering the heart to be more resilient to temporary loss of oxygenated blood flow by spurring the growth of additional blood vessels, over and above those that normally exist.
The reason heart muscle dies in a heart attack is that it becomes starved of oxygen - a heart attack is caused by blockage of an artery supplying the heart. If heart muscle had an alternative blood supply, more muscle would remain intact, and heart function would be preserved. Many researchers have therefore been searching for ways to promote the formation of additional blood vessels in the heart. "We found that a protein called RBPJ serves as the master controller of genes that regulate blood vessel growth in the adult heart. RBPJ acts as a brake on the formation of new blood vessels. Our findings suggest that drugs designed to block RBPJ may promote new blood supplies and improve heart attack outcomes."
"Studies in animals have shown that having more blood vessels in the heart reduces the damage caused by ischemic injuries, but clinical trials of previous therapies haven't succeeded. The likely reason they have failed is that these studies have evaluated single growth factors, but in fact building blood vessels requires the coordinated activity of numerous factors. Our data show that RBPJ controls the production of these factors in response to the demand for oxygen. We used mice that lack RBPJ to show that it plays a novel role in myocardial blood vessel formation (angiogenesis) - it acts as a master controller, repressing the genes needed to create new vessels. What's remarkable is that removing RBPJ in the heart muscle did not cause adverse effects - the heart remained structurally and functionally normal in mice without it, even into old age."
RBPJ is a promising therapeutic target. It's druggable, and our findings suggest that blocking it could benefit patients with cardiovascular disease at risk of a heart attack. It may also be relevant to other diseases. Inhibitors of RBPJ might also be used to treat peripheral artery disease, and activators might be beneficial in cancer by inhibiting tumor angiogenesis."
Link: http://www.eurekalert.org/pub_releases/2016-06/spmd-sbm062716.php
I've often thought a similar approach might be useful in fighting dementia (particularly vascular dementia or "normal" aging dementia) and stroke risk by creating new blood vessels in the brain, rather than trying to deal with the occluded or stiff existing vessels in the area.