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Scientists have established the cause of the lack of ability to regenerate the cells of the heart muscle
Last reviewed: 23.04.2024
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Stem cell researchers at the University of California, Los Angeles, established why adult cardiac muscle cells - cardiomyocytes - have lost the ability to proliferate, and perhaps explained why the human heart is so limited in its ability to regenerate.
A study conducted on cell lines and mice can lead to the development of methods for reprogramming cardiomyocytes directly in the heart of patients that will create a new muscle and repair damage, says Dr. Robb MacLellan of the Center for Regenerative Medicine and Stem Cell Research Eli and Edith Brody (Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research) with UCLA.
Unlike newts and salamanders, the adult body can not spontaneously repair damaged organs, such as the heart. However, recent studies show that mammals have the ability to regenerate the heart for a very short period of time - within the first week of life. Then this ability is lost. But if it was once, then maybe it will be restored?
Published in the reviewed Journal of Cell Biology, a study by Dr. McLellan shows that it is possible to return the needle of the cell clock by the time the cardiomyocytes had the ability to proliferate and restore the heart muscle.
"The salamanders and other lower organisms have the ability to dedifferentiate their cardiomyocytes, or to return them to an earlier, more primitive state, allowing these cells to return to the cell cycle, creating a new cardiac muscle," says Dr. McLellan, associate professor of cardiology and physiology. "In mammals, this potential is lost. If we knew how to restore it, or knew the reason why adult cardiomyocytes do not proliferate, we could try to find a way to regenerate the heart, using the methods of Nature itself. "
Cardiomyocytes are derived from stem progenitor cells, or progenitor cells that form the heart as a result of proliferation. Once the heart is formed, the immature myocytes are transformed into mature cells that are no longer able to reproduce. In Tritons and Newts, the situation is different: their cardiomyocytes can return to an immature or primitive state and, once again acquire the ability to proliferate, repair the damage, and then turn back into mature cells.
According to Dr. McLellan, the reason that human cardiomyocytes are not able to do the same is quite simple: in a more primitive state, cardiomyocytes lose the ability to contract normally, which is vital for the proper functioning of the heart. Since a person is much larger than newts and salamanders, in order to maintain optimal blood pressure and normal blood circulation, our heart should have been much more effective.
"In the process of our evolution, in order to maintain optimal blood pressure and circulation, we had to give up the ability to regenerate the heart muscle," says McLellan. "Our winnings are more effective cardiomyocytes and heart. But this was a compromise. "
Dr. McLellan believes that the temporary suppression of protein expression blocking the mechanism of the cell cycle may allow adults to return to the cell cycle, that is, proliferation. These methods must have reversible effects so that the effect of the effect on the proliferation-related proteins disappears after the repair of the lesion. Then the cardiomyocytes will again turn into mature cells and begin to help the restored cardiac muscle to contract. In order to knock out proteins that support myocytes in their mature state, Dr. McLellan is already considering using nanoparticles to deliver small interfering RNA into the heart.
With myocardial infarction, part of the heart stops being supplied with oxygen, and cardiomyocytes die, replaced by scar tissue. It is not difficult to find a damaged area of the heart, and if a method for reprogramming the patient's own myocytes is developed, a system controlling the activity of the desired protein and able to return the myocytes to a primitive state can be introduced into the damaged area. This allows you to replace the dead heart muscle alive.
"The ability of lower organisms to regenerate and why this does not occur in humans has long been said. This is the first article that explains why this is the case, "Professor McLellan commented on his work.
The use of human embryonic stem cells (hESCs) or reprogrammed induced pluripotent stem cells (iPSCs) for heart regeneration has been a subject of much discussion. However, it is not known what degree of regeneration can be achieved and how important the benefits from their use may be.
"From my point of view, this is a potential mechanism for the regeneration of the heart muscle without the use of stem cells," says Dr. McLellan. "In this case, each person will become a source of cells for his own regeneration."
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