As people grow older, many parts of the body gradually become stiffer and less flexible. Muscles, joints, and blood vessels can all lose some of their elasticity over time. The same thing also happens inside the heart.
For many older adults, this stiffening of the heart can lead to a serious condition called heart failure with preserved ejection fraction, also known as HFpEF. This type of heart failure is becoming increasingly common around the world, especially among aging populations.
Unlike some other forms of heart failure, the heart in HFpEF can still pump blood outward normally. The problem is that the heart muscle becomes too stiff to relax properly between beats.
Because the heart cannot relax fully, it struggles to fill with enough blood before pumping again. This can reduce blood flow throughout the body and lead to symptoms such as shortness of breath, fatigue, swelling, dizziness, and difficulty exercising.
HFpEF is especially challenging because it often occurs alongside other health problems such as high blood pressure, obesity, and high blood sugar levels. These additional conditions make the disease more complicated and harder to treat.
Despite years of research, there are still very few effective treatments that clearly reduce the risk of death in patients with HFpEF. Scientists around the world have been searching for new ways to target the underlying causes of the disease rather than simply managing symptoms.
Now, researchers at the Max Delbrück Center in Berlin, led by Professor Michael Gotthardt, together with scientists from the University of Arizona, may have found a promising new approach.
In a recent study published in the journal Cardiovascular Research, the team developed a new experimental drug called RBM20-ASO. The researchers found that the treatment improved heart function in mice with HFpEF, even when the animals also had other common health problems linked to the disease.
The scientists wanted to create a study that reflected the real-life complexity of HFpEF in humans. Instead of studying only heart stiffness alone, they tested the drug in mice that also had conditions such as obesity, high blood pressure, or blood sugar problems. This made the research model much more similar to what doctors see in actual patients.
The drug itself works in a very unusual and advanced way. RBM20-ASO belongs to a class of treatments known as antisense oligonucleotides, often shortened to ASOs.
An ASO is a small piece of genetic material designed to target specific molecules inside cells. Instead of acting like traditional drugs that affect chemicals or receptors, ASOs can influence how genes and proteins function.
In this case, the drug targets a protein called RBM20. This protein plays a major role in controlling how heart muscle cells produce another giant protein called titin.
Titin is one of the largest proteins found in the human body. It acts like a spring inside heart muscle cells. Some forms of titin are stiff, while others are softer and more flexible. The balance between these forms helps determine how stiff or stretchy the heart muscle becomes.
The researchers discovered that by lowering RBM20 levels, the heart began producing more of the softer and more elastic version of titin. As a result, the heart muscle became more flexible and better able to relax between beats.
The results in mice were encouraging. After treatment with RBM20-ASO, the animals showed improved heart relaxation and better filling of the heart chambers with blood. Importantly, the treatment improved flexibility without weakening the heart’s pumping strength.
Even in animals with multiple health problems linked to HFpEF, the drug still helped protect heart function.
The team also carefully studied how much of the drug was needed to produce benefits while minimizing side effects. They found that reducing RBM20 levels by about 50% was enough to significantly improve heart relaxation.
This moderate reduction appeared to provide a good balance between effectiveness and safety.
Any side effects seen in the mice were mild. The researchers believe side effects may be reduced even further by adjusting how often the drug is given.
Professor Gotthardt and his colleagues believe RBM20-ASO could eventually become a completely new type of treatment for HFpEF. The therapy may one day be used on its own or combined with existing medications to better protect the heart and slow disease progression.
However, the drug is still in the experimental stage and has not yet been tested in humans. Before human trials can begin, the researchers plan to study the treatment in pigs, whose hearts are more similar to human hearts in size and structure.
If future studies are successful, the therapy could bring hope to millions of older adults living with HFpEF, a condition that currently has very limited treatment options.
The findings are especially important because HFpEF continues to rise as populations age worldwide. Researchers hope that targeting the mechanical stiffness of the heart itself may finally offer a more direct and effective way to treat this difficult disease.
Although more work is still needed, the study marks an exciting step forward in the search for better heart failure treatments and healthier aging.
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The study is published in Cardiovascular Research.
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