As people get older, the muscles in their body begin to stiffen—including the heart.
This can lead to a common type of heart failure where the heart still pumps blood but struggles to relax and fill between beats.
Known as heart failure with preserved ejection fraction (HFpEF), this condition affects many older adults.
Yet until now, there hasn’t been an effective treatment that reduces the risk of death in patients with this kind of heart failure.
Professor Michael Gotthardt and his team at the Max Delbrück Center in Berlin, together with collaborators from the University of Arizona, are working to change that.
In a recent study published in Cardiovascular Research, the team showed that a drug they developed—called RBM20-ASO—can improve heart function in mice with HFpEF.
HFpEF is more than just a stiff heart. Many patients also have other conditions like high blood pressure, obesity, or high blood sugar. These additional health problems make HFpEF more complicated and harder to treat.
To reflect this, the researchers tested their new drug in mice that had both HFpEF and these common comorbidities. This approach helped them better mimic how the disease works in humans.
The drug RBM20-ASO is a type of molecule known as an antisense oligonucleotide, or ASO for short. It’s a small, single-stranded piece of genetic material that targets a specific protein called RBM20.
This protein helps control how heart muscle cells build a giant protein named titin. Titin works like a spring in heart muscle—some forms are stiff and others are elastic. The drug reduces RBM20 levels, causing heart cells to make more of the softer, stretchier version of titin.
The results were promising. After receiving the treatment, the mice had hearts that were more flexible and better able to fill with blood. This improved the heart’s ability to function without weakening its strength. Even with other health problems present, the drug helped the heart stay healthy.
The study also looked at how much of the drug is needed to get results while keeping side effects low. The researchers found that only a moderate reduction in RBM20 levels—around 50%—was enough to make a difference.
This allowed the heart to relax better without harming its ability to pump. Any side effects observed in the animals were mild, and the team believes they can reduce these further by changing how often the drug is given.
Gotthardt and his team believe that RBM20-ASO has the potential to be a new treatment for HFpEF. It may be used alone or together with other therapies to help restore the heart’s ability to relax and prevent further damage. Before it can be tested in humans, though, the drug will go through additional studies in pigs, which have hearts more similar to ours.
If these upcoming studies are successful, this therapy could offer new hope for millions of aging adults struggling with heart failure that has so far lacked effective treatments.
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The study is published in Cardiovascular Research.
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