Can heart attacks be reversed now?- edited by Aishee Biswas

Our hearts are constantly working to keep us alive, but unfortunately, they are not very efficient at self-repair. This often leads to a buildup of scar tissue after a heart attack, which can significantly impact the heart's ability to function properly. However, researchers have found inspiration in the way young hearts heal themselves and have developed a technique to convert scar tissue into healthy tissue in mice. This breakthrough offers hope for reducing the damage caused by heart attacks and improving heart function. Preventing and minimizing the damage caused by heart attacks is a major priority for scientists in the United States where someone experiences a heart attack every 40 seconds. Although significant research has been conducted into the prevention of heart attacks, there is now a growing focus on repairing the heart after it has been damaged, particularly the scar tissue that forms after a heart attack. 

 

The scar tissue is more rigid than healthy heart tissue and can restrict the heart's proper functioning and lead to future complications. Therefore, there is an urgent need to  develop strategies to address this issue  and improve the overall health outcomes of patients who have suffered from heart attacks.
 

Earlier this year, a team of scientists in Australia discovered a method to combat heart scarring in rats by boosting elastin, a substance that provides some tissues with their elastic qualities. The study found that the scar tissue in the heart reduced in size and became more flexible, allowing the heart to regain almost normal function.

 

Building on this research, scientists at Duke University aimed to use cellular reprogramming, a process involving RNA, to convert fibroblasts, cells responsible for forming connective and scar tissue, into healthy heart tissue after a heart attack. The technique has been studied previously for restoring motor function in stroke victims, wound repair, and other purposes, in addition to heart repair efforts.

However, in their studies with mice,  the researchers discovered that adult fibroblast cells were not as receptive to reprogramming as juvenile fibroblasts . The team identified that a protein oxygen sensor called Epas1 was responsible for preventing adult cells from responding to the reprogramming instructions. To enable successful transformation of the adult cells, the researchers inhibited Epas1.

 

The study's significance extends beyond heart repair. The researchers not only utilized cellular reprogramming but also found a way to counteract the effects of aging on some cells. As a result, the implications of the findings could extend to other medical fields, such as the regeneration of neurons in the brain and the reversal of skin scarring in specific dermatological conditions.