Human Heart Has Potential to Self-Repair After Cardiac Attack Using Specific Cells, Confirms New Study
In a new research, it has been revealed that the body’s immune response and the lymphatic system (a part of the immune system) are critical in the heart’s ability to repair itself after an attack. These macrophages release a specific sort of protein called VEGFC as the first responders on the scene after a heart attack.
When it comes to self-healing mechanisms, we are blessed with a body that can take care of itself. Scientists have been researching the manner in which the heart repairs itself after an attack. They aim to uncover insights that will lead to more effective cardiovascular therapy. In a new research, it has been revealed that the body’s immune response and the lymphatic system (a part of the immune system) are critical in the heart’s ability to repair itself after an attack has damaged the cardiac muscle. The revelation of the function performed by macrophages — the specialised cells that can eliminate bacteria or generate beneficial inflammation responses — was crucial to the study.
These macrophages release a specific sort of protein called VEGFC as the first responders on the scene after a heart attack. The researchers discovered that macrophages, or the immune cells that rush to the heart after an attack to “eat” injured or dead tissue, also produce vascular endothelial growth factor C (VEGFC), which aids healing by triggering the development of new lymphatic capillaries.
The researchers characterise it as a Jekyll and Hyde situation, with the good macrophages making VEGFC and the bad ones not producing VEGFC but causing a pro-inflammatory response that can injure the heart and surrounding tissue even more.
Dying cells must be cleaned away for the heart to fully mend itself, a process known as efferocytosis in which macrophages play a key role. The scientists discovered how the right type of VEGFC-producing macrophages accomplished a proper repair job by studying the process in lab cells and animals.
“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 process of heart repair,” said pathologist Edward Thorp from Northwestern University in Illinois.
The findings of the study were reported in the Journal of Clinical Investigation.
Future studies could focus on ways to improve the number of beneficial macrophages in the heart while lowering – or even eliminating – the number of harmful macrophages, increasing the chances of a successful recovery.
Northwestern University vascular scientist Guillermo Oliver said that they were trying to figure out how heart failure developed after a cardiac attack so that they can intervene early and get the heart back on track.
While scientists continue to advance their understanding of how cardiovascular disease is caused and how to better assess the risk of heart problems sooner, cardiac failure continues to kill lakhs of people worldwide every year.
