Biologists have found a gene responsible for heart regeneration

Biologists have found the gene responsible for the regeneration of the heart. The work of an international group of scientists from the UK, Germany and Austria is published in the journal Nature Communications.

The cell cycle, the process by which cells copy themselves, is strictly controlled by the mammalian organism. For example, cancer develops when cells begin to multiply uncontrollably.

A key role in this process is played by a gene called Myc, which becomes hyperactive in most cancers. Therefore, his research is the main focus of scientists who are trying to stop the development of cancer.

In a new study, scientists analyzed the activation of the Myc gene based on various organs (heart, kidney, and liver) in the mouse. Gene activation has led to a significant increase in the number of cells in these organs.

Analyzing the heart of mice, the researchers concluded that the Cyclin T1 protein, which is produced by the Ccnt1 gene, is responsible for Myc hyperactivity in this organ.

“When these two genes were co-overexpressed in the heart muscle cells of adult mice, we saw extensive cell replication, which led to a significant increase in the number of heart muscle cells. This is really exciting because scientists have long been trying to get heart cells to multiply, but not one of the modern methods of treating heart disease can reverse the degeneration of heart tissue. All of them only slow down the progression of the disease. Now we have found such a method in a mouse model”.

Katherine Wilson, lead author of the study

The discovery will accelerate the recovery of the heart after attacks, during which the muscle loses many cells. However, prior to testing the method in humans, it is necessary to conduct additional experiments to evaluate its safety, the authors of the study note.

Author: Flyn Braun
Graduated from Cambridge University. Previously, he worked in various diferent news media. Currently, it is a columnist of the us news section in the Free News editors.
Function: Editor