More than 64 million people around the world live with heart failure. In the United States alone, about 6.7 million people have this serious condition.
Heart failure happens when the heart becomes too weak or stiff to pump blood properly. This can lead to tiredness, shortness of breath, and even death.
For a long time, the main way to treat heart failure has been to manage the symptoms with medicine. But these treatments don’t fix the root causes of the problem.
Now, scientists at The Ohio State University College of Medicine have made an exciting discovery. They found a new way to help hearts heal from damage and stress. The researchers focused on a special protein in the heart called CPT1a. This protein helps heart cells get energy. It also seems to protect the heart when it is under stress.
The team discovered that when the heart is not working well, it naturally makes more of this protein. So, they asked a big question: what if we could boost the amount of CPT1a even more to help the heart recover? To test this idea, they used gene therapy—a method that changes the way cells work by adding helpful genes.
They gave this therapy to mice with heart problems. The results were amazing. The mice that got more CPT1a had better heart function. Even mice that were already sick showed improvement. On the other hand, mice that couldn’t make enough CPT1a got worse faster. This showed that CPT1a plays a very important role in keeping the heart strong.
The scientists also studied real human heart samples from people with a condition called nonischemic cardiomyopathy, or NICM. This disease makes it hard for the heart to pump blood, but it’s not caused by blocked arteries.
They compared the hearts of NICM patients to healthy donor hearts. In the NICM group, both men and women had higher levels of CPT1a. Another related protein, CPT1b, did not increase. This finding confirmed that CPT1a might be the key player in the body’s natural defense system against heart failure.
The researchers also found that CPT1a does more than just help the heart make energy. It also stops harmful genes that cause scarring and cell death. This means CPT1a could help stop the heart from getting worse over time.
This research was led by Dr. E. Douglas Lewandowski, who is a senior scientist at Ohio State’s Heart and Lung Research Institute. He believes this new gene therapy could become a powerful treatment. Unlike drugs that people must take every day, this could be a one-time treatment that helps the heart for a long time.
Dr. Lewandowski and his team are now working on more tests in animals. They hope to start testing this therapy in humans in the future. He and Dr. Andrew Carley, also from Ohio State, have even applied for a patent on this new method.
This study gives hope to millions of people living with heart failure. If gene therapy can boost the heart’s own healing system, it might change the way we treat heart disease. Instead of just treating symptoms, doctors could help fix the damage and give patients a better quality of life.
The results of this study were published in the journal Circulation Research. The findings are exciting because they offer a new way to look at heart failure treatment. For many years, researchers have tried to find better ways to help the heart heal. Now, this gene therapy using CPT1a might be a big step forward.
In summary, this research shows that the heart already tries to protect itself by making more CPT1a.
Helping it do that with gene therapy could stop heart failure from getting worse. It could also help the heart recover from stress and damage. This new treatment might one day offer people a longer and healthier life, with fewer medicines and better results.
If you care about heart disease, please read studies about a big cause of heart failure, and common blood test could advance heart failure treatment.
For more health information, please see recent studies about a new way to repair human heart, and results showing drinking coffee may help reduce heart failure risk.
The study is published in Circulation Research.
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