The human heart can repair itself and we already know which cells are crucial

Our body, specifically our organs, is very resourceful when it comes to self-repair. In this sense, scientists have studied in detail how the heart repairs itself after a heart attack (myocardial infarction). Scientists hope to find clues that could lead to better treatments for cardiovascular problems.

New research has revealed that the immune response of the body and the lymphatic system (part of the immune system) is crucial in how the heart repairs itself after a heart attack.

Does our heart have the power to repair itself?

The key to the study was the discovery of the role played by macrophages, specialized cells that can destroy bacteria or initiate helpful inflammatory responses. As first responders in a post-heart attack scene, these macrophages produce a particular type of protein called VEGFC, the researchers report.

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) which triggers the formation of new lymphatic vessels and promotes healing.

Explained pathologist Edward Thorp of Northwestern University in Illinois.

Researchers describe it according to a scenario of Jekyll and Hyde: the "good" macrophages which produce VEGFC and the "bad" macrophages which do not produce VEGFC but cause pro-inflammatory response that can cause more damage to the heart and surrounding tissues.

For the heart to fully repair itself, dying cells must be removed - a process known as efferocytosis in which macrophages play an important role. By studying this process in cells in the lab and in mice, the team identified how the right kind of VEGFC-producing macrophages did the right repair work.

What future research might look for next is how to increase the number of helpful macrophages in the heart and reduce the number – or even eliminate – harmful macrophages, increase the chances of a healthy recovery.

Our challenge now is to find a way to deliver VEGFC or persuade these macrophages to induce more VEGFC to speed up the repair process of the heart.

said Thorp.

26 million people currently live with heart failure

When people are struck by a heart attack, they are at high risk of heart failure, where the heart is unable to continue pumping blood throughout the body. This risk can be reduced with modern drugs like beta-blockers, but it is still there.

As scientists continue to improve our understanding of the cause of cardiovascular disease and how we can better and earlier diagnose the risk of heart problems, heart failure continues to kill hundreds of thousands of people every year. According to the Portuguese Society of Cardiology, heart failure (HF) is a growing public health problem. Around 26 million people worldwide are currently living with HF.

Further studies like this will shed more light on the biological processes that occur in response to a heart attack – in particular how the process of efferocytosis is used to trigger the protein VEGFC needed for heart muscle repair.

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