The human heart can repair itself, and now we know which cells are important for it to do so
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Our bodies are very adept when it comes to self-repair.
And scientists have studied in detail the ways the heart repairs itself after a heart attack (myocardial infarction).
They hope to find clues that could lead to better treatments for cardiovascular problems.
New research has revealed that the body’s immune response and the lymphatic system (part of the immune system) are essential in the way the heart repairs itself after a heart attack that damaged heart muscle.
Key to the study was discovering the role played by macrophages, specialized cells that can destroy bacteria or initiate beneficial inflammatory responses.
The researchers reported that these macrophages, as first responders on the scene after a heart attack, produce a specific type of protein called VEGFC.
“We found that macrophages, or immune cells that rush into the heart after a heart attack to ‘feed’ damaged or dead tissue.
It also stimulate vascular endothelial growth factor C (VEGFC) which stimulates new lymphatic vessel formation and promotes healing,” says pathologist Edward Thorpe of Northwestern University in Illinois.
The researchers describe it as a Jekyll and Hyde scenario:
Good Macrophages
“good” macrophages produce VEGFC and
Bad Macrophages
“bad” macrophages do not produce any VEGFC but cause a pro-inflammatory response that can cause more damage to the heart and surrounding tissues.
Efferocytosis
In order for the heart to fully repair itself, the dying cells must be removed – a process known as efferocytosis in which macrophages play an important role.
By studying this process in cells, in vitro and in mice.
The team determined the way in which the correct type of VEGFC-producing macrophage did a proper repair job.
What future research could investigate next is
1) How to increase the number of beneficial macrophages in the heart and reduce the number – or
2) Even eliminate – harmful macrophages, enhancing the chances of a healthy recovery.
“Our challenge now is to find a way to either administer VEGFC or coax these macrophages to induce more VEGFC, in order to speed up the repair process of the heart,” says Thorpe.
When people have a heart attack, they are more likely to develop heart failure, in which the heart becomes unable to pump blood throughout the body.
This risk can be reduced with the use of modern medications such as beta-blockers, but it is still present.
As scientists continue to improve our understanding of how cardiovascular disease occurs, and how we can better diagnose heart disease risk earlier.
As heart failure continues to kill hundreds of thousands of people annually in the United States alone.
Further studies like this one will shed more light on the biological processes that occur in response to a heart attack.
In particular the way in which the process of pluripotency is used to stimulate the VEGFC protein required for heart muscle repair.
“We are working to understand more about the development of heart failure after a heart attack, in order to intervene early and reset the course of heart repair,” says vascular biologist Guillermo Oliver of Northwestern University.
