New study sheds light on heart regeneration mechanism in zebrafish
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Understanding how the heart heals after a heart attack has been a key area of study in medical science. And one research model that could help us understand heart regeneration is the zebrafish.
After suffering cardiac damage, zebrafish have the superpower to repair heart muscles within 90 days naturally. Jeroen Bakkers' (Hubrecht Institute, Netherlands) research group has focused on unraveling how zebrafish fully restore their cardiac function.
Zebrafish heart damage recovery
This unique ability stems from heart muscle cells' ability to divide and form more cells, allowing faster recovery. This way, the damaged heart cells are replaced by newer ones. However, how the cells stop dividing after the heart is restored has remained a mystery.
“It is unclear how these cells stop dividing and mature enough to contribute to normal heart function. We were puzzled by the fact that in zebrafish hearts, the newly formed tissue naturally matured and integrated into the existing heart tissue without any problems,” said Phong Nguyen, the study's first author, in an official statement.
The researchers cultured slices of damaged heart cells outside zebrafish bodies to better understand the underlying factor. This laboratory examination of the cellular process revealed a "switch" mechanism for heart muscle cells.
The interplay of calcium
They discovered that the flow of calcium within heart muscle cells determines heart contractions, which could predict cell maturity in zebrafish. According to the statement, the calcium movements in and out of cells changed over time as the cells matured.
“The calcium movement in the newly divided cell was initially very similar to embryonic heart muscle cells, but over time the heart muscle cells assumed a mature type of calcium movement. We found that the cardiac dyad, a structure that helped to move calcium within the heart muscle cell, and specifically one of its components, LRRC10, was crucial in deciding whether heart muscle cells divide or progress through maturation. Heart muscle cells that lack LRRC10 continued to divide and remained immature,” explained Nguyen.
The study concluded that the LRRC10 gene may be essential in reducing cell division and increasing heart muscle cell maturation.
In the next step, the team applied their findings to mouse and lab-grown human heart muscle cells by inducing LRRC10. The results showed that genes in mammals regulated calcium movement like that seen in zebrafish hearts.
“It was exciting to see that the lessons learned from the zebrafish were translatable as this opens new possibilities for the use of LRRC10 in the context of new therapies for patients,” added Nguyen.
This understanding could lead to the development of therapies for cardiovascular disease, which is a leading cause of death worldwide.
The new study results have been reported in the journal Science.
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