In a recent study, researchers have pinpointed a hidden culprit that leads to dilated cardiomyopathy—a dangerous condition that accounts for 20 percent of all cases of heart failure.
The finding opens the door to potential new treatments that could help counter the threat.
The study was conducted by an international research team led by scientists at the University of Alberta.
The team identified a key molecule named PI3K alpha that binds to gelsolin—an enzyme that can destroy filaments that help make up the structure of the heart’s cells—and suppresses it.
The researchers believe the molecule holds great promise as a possible therapeutic target, offering a possible path forward to personalized and precision medicine for patients with dilated cardiomyopathy.
The condition decreases the heart’s ability to pump blood because its main pumping chamber, the left ventricle, is enlarged and weakened.
The researchers studied the condition at the molecular level in animal models and in explanted human hearts and found that the pathway leading to dilated cardiomyopathy is common in all species.
According to the team, the condition is caused by biomechanical stress, which activates the gelsolin enzyme.
People need some gelsolin, but when it gets out of control, it destroys things.
The molecule chews up the filaments and people get really bad heart failure.
But the team has also shown that when people suppress this molecule, they could preserve the heart function. It’s intact.
The potential impact on patient care is huge. By understanding these patients better, the team hopes to develop specific therapies for them.
there are currently no specific treatments for patients with heart failure. The same medications are used for all patients.
If doctors can now identify patients that have problems with this type of remodeling (dilated cardiomyopathy), they can target them specifically.
That’s where the researchers are heading down the road. And to take this research right from the molecule to the patients, the team says it’s very rewarding.
The research is published in Nature Communications.
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