The Human Heart Can Repair Itself, And We Now Know Which Cells Are Crucial For It

When it comes to self-repair, our bodies are very creative, and scientists have been examining the manner in which the heart repairs itself after a heart attack in great detail (myocardial infarction). They hope to unearth signs that will lead to new therapies for cardiovascular ailments.

According to new study, the immunological response of the body and the lymphatic system (part of the immune system) are critical in the way the heart heals itself after a heart attack has caused damage to the heart muscle.

The finding of the function performed by macrophages, specialised cells that may eliminate germs or induce beneficial inflammatory responses, was critical to the study. These macrophages release a specific sort of protein called VEGFC as the first responders on the scene after a heart attack, according to the researchers.

"We found that macrophages, or immune cells that rush to the heart after a heart attack to 'eat' damaged or dead tissue, also induce vascular endothelial growth factor C (VEGFC) that triggers the formation of new lymphatic vessels and promotes healing," says pathologist Edward Thorp of Northwestern University in Illinois.

The researchers characterize it as a Jekyll and Hyde scenario, with 'good' macrophages making VEGFC and 'bad' macrophages not producing VEGFC but creating a pro-inflammatory response that can injure the heart and surrounding tissue even more.

To effectively mend the heart, dying cells must be swept away, a process known as efferocytosis in which macrophages play a crucial role. The scientists discovered how the correct sort of VEGFC-producing macrophages accomplished a proper repair job by studying this process in lab cells and animals.

Future study might look at methods to raise the amount of good macrophages in the heart while decreasing – or perhaps eliminating – the number of detrimental macrophages, increasing the odds of a successful recovery.

"Our challenge now is to find a way either to administer VEGFC or to coax these macrophages to induce more VEGFC, in order to speed the heart repair process," Thorp adds. 

People who have a heart attack are at a significant risk of developing heart failure, in which the heart is unable to continue pumping blood around the body. That danger can be minimized with contemporary medications such as beta-blockers, but still remains.

While scientists continue to advance our understanding of how cardiovascular disease develops and how we might better detect the risk of heart issues sooner, heart failure continues to kill hundreds of thousands of individuals in the United States each year.

More research like this one will provide more insight on the biological processes that occur in response to a heart attack, specifically how the mechanism of efferocytosis is employed to activate the VEGFC protein, which is essential for heart muscle healing.

"We are working to understand more about the progression to heart failure after a heart attack, in order to intervene early and reset the course to cardiac repair," explains Northwestern University vascular scientist Guillermo Oliver.