When comes to self-healing mechanisms, we are lucky to have a body that can take care of itself. Scientists have been studying the way the heart repairs itself after an attack. They aim to discover insights that will lead to more effective cardiovascular treatments. In a new study, it has been revealed that the body’s immune response and the lymphatic system (part of the immune system) are critical to the heart’s ability to repair itself after an attack on the heart muscle. The function of macrophages—specialized cells that can eliminate bacteria or generate a beneficial inflammatory response—was critical to the study.

These macrophages release a specific protein called VEGFC as first responders on the scene after a heart attack. The researchers found that macrophages, or 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 helps by triggering the development of new lymphatic capillaries. heal.

Described by the researchers as the case of Jekyll and Hyde, good macrophages produce VEGFC, while bad macrophages do not, but cause a pro-inflammatory response that causes more damage to the heart and surrounding tissue .

Dying cells must be removed before the heart can fully repair itself, a process known as pleocytosis, in which macrophages a key role. By studying the process in laboratory cells and animals, the scientists discovered how the right type of VEGFC-producing macrophages does the proper repair work.

“Our challenge now is to find a way to manage VEGFC or induce these macrophages to induce more VEGFC to speed up the cardiac repair process,” said pathologist Edward Thorp of Northwestern University in Illinois.

See also  NASA confirms DART mission test successfully changed asteroid Dimorphos' orbit by 32 minutes: all the details

The results of the study were published in the Journal of Clinical Investigation.

Future research may focus on methods to increase the of beneficial macrophages in the heart, while reducing or even eliminating the number of harmful macrophages, thereby increasing the chances of a successful recovery.

They’re trying to figure out how heart failure develops after a heart attack so they can intervene early and get the heart back on track, says Northwestern University vascular scientist Guillermo Oliver.

While scientists continue to deepen their understanding of how cardiovascular disease is caused and how to better assess heart disease risk faster, heart failure continues to kill hundreds of thousands of people worldwide each year.