Scientists at the Max Delbrück Center for Molecular Medicine (MDC) have identified a mechanism that allows zebrafish to fully repair the heart muscle after a heart attack. The discovery could form the basis of drugs for heart regeneration in humans. The research was published in the journal Developmental Cell.
The human heart cannot produce new heart cells; instead, scar tissue replaces the muscle (myocardium) damaged by the heart attack. This impairs the heart’s ability to contract. In a new study, scientists have identified a mechanism that could trigger myocardial regeneration after a heart attack.
It is known that the autonomic nervous system and immunity, especially immune cells macrophages, play key roles in regeneration during heart attack. In the new study, scientists conducted experiments on zebrafish larvae that were able to completely repair damaged heart muscle. In the early stages of development, these animals are transparent and therefore suitable for study.
The biologists induced myocardial damage in zebrafish and also blocked several molecules on the surface of macrophage immune cells that play an important role in heart regeneration. This allowed biologists to figure out which molecules are responsible for the connection between the nervous system and the immune system as they work together to repair the heart muscle. Blocking these molecules prevented macrophages from moving to the site of myocardial injury. This impaired heart muscle regeneration in fish and initiated the scarring process.
Now scientists plan to investigate how the transmission of signals from the nervous system to the immune system differs between zebrafish and humans. This will help understand why heart muscle tissue fails to regenerate in humans and identify molecules that will become targets of drugs that repair the heart after a heart attack.
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