Reactivating a Dormant Gene Could Reverse Heart Attack Damage

Heart attack damage is not only dangerous during the initial event but also due to the long-term effects that follow. Researchers have now identified a dormant gene that, when reactivated, could regenerate heart tissue and potentially prevent heart failure.

After a heart attack, scar tissue forms to maintain the organ’s structure. However, this tissue lacks the ability to contract, which can disrupt the heart’s rhythm. Over time, this dysfunction increases the risk of further heart attacks and eventual heart failure.

Zebrafish: A Model for Heart Regeneration

Interestingly, not all species share this limitation. Zebrafish, for instance, can regenerate damaged heart tissue as easily as healing a surface wound, fully restoring heart function within just 60 days of injury—a remarkable ability that scientists are eager to explore further.

In a recent study, researchers at the Hubrecht Institute in the Netherlands identified a protein involved in heart tissue repair in zebrafish. They then tested this protein on mouse hearts, which also lack natural regeneration, and observed promising results, indicating the potential for similar treatments in humans.

We analyzed gene activity in damaged and healthy heart tissues,explained Dennis de Bakkers, the study’s lead author. Our findings showed that the gene responsible for producing the Hmga1 protein is active during heart regeneration in zebrafish but inactive in mice. This suggests that Hmga1 plays a crucial role in heart repair.

Successful Gene Transfer in Mice

To test whether this regenerative mechanism could be transferred, the researchers used a viral vector to deliver the Hmga1 gene to damaged heart tissue in live mice. The results were encouraging: heart muscle cells began to divide and grow, significantly improving cardiac function.

There were no side effects, such as excessive growth or an enlarged heart,” noted Mara Bouwman, co-lead author of the study. “We also didn’t observe any cell division in healthy heart tissue. This indicates that the damage itself triggers the regenerative process.

While these findings are promising, results from mouse studies do not always translate directly to humans. However, there is reason for optimism in this case. The gene coding for Hmga1 is still present in humans, remaining active during embryonic development before becoming dormant after birth. Reactivating this gene could offer a way to repair heart damage following a heart attack.

The next step in the research involves testing the effect of the Hmga1 protein on human heart muscle cells grown in the lab, bringing the potential treatment one step closer to reality.

Read the original article on: New Atlas

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