Towards the first curative treatment for heart disease

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S.Mencía

Madrid

Updated:04/14/2020 13:05

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Trying to deactivate a gene that facilitates the spread of cancer, a team of researchers from the Cambridge University (UK) have made a surprising finding. By making the Myc gene is hyperactive and functional in the hearts of mice, they have triggered the regeneration of heart cells. Because adult hearts generally cannot repair themselves once damaged, scientists believe that taking advantage of power of this gene represents a breakthrough towards the first curative treatment for heart disease.

“This is really exciting because for years we have been trying to make heart cells proliferate. None of the current treatments for heart disease can reverse the degeneration of heart tissue; they only slow the progression of the disease. Now we have discovered a way to do it in a mouse model, ”explains Catherine Wilson, researcher at the Department of Pharmacology at the University of Cambridge, and director of the study.

The cell cycle, through which cells make copies of themselves, is strictly controlled in mammalian cells. Cancer develops when cells begin to replicate uncontrollably, and the Myc gene plays a key role in the process. Myc is known to be hyperactive in the vast majority of cancers, so attack this gene it is a top priority in cancer research. Many current studies for cancer treatment have focused on trying to control Myc.

When the Ccnt1 and Myc genes are expressed together, the heart changes to a regenerative state and its cells begin to replicate.

In the study that is now published in Nature Communications, when researchers made Myc was hyperactive in a mouse model And, as they expected, they saw its cancerous effects on organs such as the liver and lungs: large numbers of cells began to replicate within a few days.

The researchers found that Myc-powered activity in heart muscle cells depends on the level of another protein called Cyclin T1, produced by a gene called Ccnt1, inside the cells. When genes Ccnt1 and Myc they express themselves together, the heart changes to a regenerative state, and its cells begin to replicate.

Heart cells – Archive

“When these two genes were overexpressed together in the heart muscle cells of adult mice, we saw a pronounced cell replication, which led to a large increase in the number of cells in the heart muscle, “says Wilson.

Heart failure affects around 23 million people worldwide each year and, currently, there is no cure. After a heart attack, an adult human heart can lose up to billion muscle cells cardiac calls cardiomyocytes. Unlike many other organs in the body, the adult heart cannot regenerate, so these cells are never replaced. Its loss reduces the strength of the heart and results in scarring, heart failure, and ultimately death.

“None of the current treatment options can reverse cardiac tissue degeneration. The inability of the heart to regenerate it’s an important unmet clinical need, ”says Wilson.

We want to use short-term interchangeable technologies to activate Myc and Cyclin T1 in the heart. In this way we will not leave any genetic fingerprint that can promote the formation of cancer.

In this study, he adds, “We discovered that even when Myc is turned on in a heart, the other tools are not there to make it work, which may be one reason why heart cancer is so extremely rare. Now we know what lack, we can add it and make cells replicate».

The researchers hope to develop their finding into a gene therapy for the treatment of heart disease. “We want to use short-term interchangeable technologies to activate Myc and Cyclin T1 in the heart. That way we won’t leave any genetic fingerprints that can promote cancer formation, “said Wilson.

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