A 2026 study in rats found that synthetic relaxin-2 reversed stiff-heart problems and stopped sustained irregular heartbeats after two weeks of treatment. Gram Research analysis of this work suggests relaxin may be a promising future target for heart failure with preserved ejection fraction, though it has not yet been tested in people.
According to research reviewed by Gram, a 2026 study in rats found that a synthetic form of the hormone relaxin-2 helped reverse a common type of heart failure. This condition, called heart failure with preserved ejection fraction (HFpEF), makes the heart muscle stiff so it cannot fill with blood properly. After two weeks of treatment, the rats’ hearts filled better, their left atrium (the upper chamber of the heart) shrank, and dangerous, long-lasting irregular heartbeats disappeared in the treated group. The study used a small number of animals and has not been tested in people. Still, the results suggest relaxin-2 may be worth studying further as a possible future treatment for this hard-to-treat condition.
Key Statistics
A 2026 animal study published in PLoS One found that after two weeks of treatment, none of the 6 rats given synthetic relaxin-2 had sustained irregular heartbeats, compared with 2 of 5 untreated high-fat diet rats.
According to research reviewed by Gram, the 2026 rat study reported that relaxin-2 treatment reduced the size of the left atrium and improved a key measure of heart stiffness in rats with heart failure with preserved ejection fraction.
The 2026 study involved 19 male rats in total, with 11 fed a high-fat diet to trigger heart failure, and found that scarring in heart tissue did not change significantly with relaxin treatment.
The Quick Take
- What they studied: Researchers asked whether a synthetic form of the hormone relaxin-2 could repair the stiff-heart problems and dangerous heart rhythms seen in a rat model of heart failure with preserved ejection fraction.
- Who participated: The study used male lab rats of a special strain that develops heart problems when fed a high-fat diet. In total, 19 rats began the study: 8 were fed a normal diet and 11 were fed a high-fat diet. Only rats that developed the heart condition were treated, and the rats were randomly assigned to receive relaxin or a placebo.
- Key finding: After treatment, the rats’ hearts filled with blood more normally, and their left atrium became smaller. Dangerous irregular heartbeats that lasted a long time were no longer seen in the relaxin group, while the untreated high-fat diet rats had them in 2 of 5 cases. Because the groups were small, these numbers are best seen as early clues rather than proof.
- What it means for you: This is early research in animals, so it does not mean relaxin is safe or useful for people today. If you have heart failure or irregular heartbeats, the best step is to keep following your doctor’s treatment plan. Relaxin-based medicines are not a standard option for this condition.
The Research Details
The researchers used a type of rat that naturally develops a condition similar to heart failure with preserved ejection fraction, especially when fed a high-fat diet. Over 11 weeks, they used repeated heart ultrasounds to check whether the rats had developed stiff hearts that struggled to fill with blood. Once the condition was confirmed, the rats were randomly assigned to receive either synthetic relaxin-2 or a placebo, delivered through small pumps implanted under the skin for two weeks.
After treatment, the researchers took more heart ultrasounds and then removed the hearts to study them directly. They used special dyes and cameras to map the electrical signals moving across the heart, and they gave the hearts electrical pulses to see whether they would develop irregular rhythms. They also examined heart tissue under a microscope and measured gene activity to understand how relaxin might be working.
Because the study compared treated rats with untreated rats at the same time, it can show cause and effect more clearly than a simple observation would. However, the groups were small, and the study was done in animals, so the results may not apply directly to humans.
Using randomly assigned groups helps reduce the chance that other differences between the rats, such as their age or weight, explain the results. Repeating the heart scans before and after treatment allowed the team to see changes in the same animals over time. Studying the heart directly after death gave a detailed look at electrical signals and tissue changes that cannot be measured easily in living people.
Animal models are an important early step because they let scientists test a new idea safely before moving to human trials. This approach can reveal how a treatment might work, which helps guide future research into whether it is safe and effective in people.
The study was published in a peer-reviewed journal, which means other scientists checked the work before publication. Its strengths include random assignment to treatment and placebo, repeated heart measurements, and detailed lab analysis. However, the number of rats in each group was very small, which makes it harder to be confident the results would hold up in larger studies. The authors also described some results as trends rather than clear, statistically strong findings. Results from a rat model also do not automatically translate to people.
What the Results Show
The clearest result was that relaxin treatment improved how the heart fills with blood. Ultrasound scans showed that the left atrium, the chamber that receives blood before it moves to the main pumping chamber, became smaller after treatment. A key measure of stiffness, called E/e’, also improved, suggesting the heart was relaxing more normally between beats.
Relaxin treatment also appeared to reduce signs of strain on the heart. Levels of a marker called NT-pro-ANP, which rises when the heart is under stress, moved closer to healthy levels in treated rats. Blood sugar and blood pressure were elevated in the high-fat diet rats, and the study describes relaxin as largely reversing the overall stress on the heart.
The most striking finding involved heart rhythm. In untreated high-fat diet rats, 2 of 5 had sustained irregular rhythms in the upper or lower chambers. In the relaxin group, none of the 6 rats had these long-lasting rhythms. However, shorter, less serious irregular beats were not clearly reduced by relaxin, and some still occurred in treated animals.
At the molecular level, relaxin was linked to changes in gene activity and proteins involved in heart cell communication and electrical signaling. Relaxin appeared to increase proteins that help electrical signals travel across the heart and to shift certain signaling pathways, such as Wnt, that are involved in tissue repair. Scarring in the heart tissue did not change significantly, which suggests the benefits did not come from reducing fibrosis in this model.
The researchers observed that relaxin tended to speed up electrical signals traveling through heart tissue, especially at faster heart rates. This may help the heart keep a steadier rhythm under stress, though the authors describe this as a trend rather than a clear, confirmed effect. Changes in gene activity pointed toward a possible role for relaxin in improving how heart cells communicate with each other. Because these were laboratory measurements in a small number of animals, they are best viewed as clues for future research rather than firm conclusions.
Relaxin has been studied before as a possible treatment for heart disease, including in human clinical trials for acute heart failure. Those earlier trials produced mixed results, and relaxin has not become a standard treatment. This new study adds to the evidence by focusing on the stiff-heart form of heart failure, which has fewer effective treatments than many other heart conditions. It also suggests a possible link between relaxin, heart rhythm, and signaling pathways that earlier research had not fully explored. Even so, it is an animal study, so it builds on rather than replaces the need for well-designed human research.
The study had a small number of animals in each group, which makes it harder to be sure the results would hold up in a larger group. Some of the most important differences were measured in tiny subgroups, such as the three rats in the normal diet group used for certain heart rhythm tests. The study used only male rats, so it is unclear whether the results would apply to females. Rats are not people, and a condition that looks similar in animals may not behave the same way in humans. The study also did not show that relaxin reduced all irregular heartbeats, since shorter episodes were not clearly improved. Finally, the study lasted only a few weeks, so it does not show whether benefits last or whether there are long-term side effects.
The Bottom Line
Based on this single animal study, the evidence is promising but early. Relaxin-2 appears to improve stiff-heart function and reduce sustained irregular heartbeats in rats, so researchers have good reason to test it in human clinical trials. People should not start or seek relaxin treatment based on this study alone. Confidence in the findings is currently low to moderate, since they come from a small animal study that has not yet been repeated or tested in people.
Heart specialists, researchers who study heart failure, and people living with heart failure with preserved ejection fraction may find this research relevant. Patients should talk to their cardiologist before making any decisions based on it. People without heart disease do not need to change their treatment or behavior because of this study. Anyone with heart symptoms should seek medical care rather than wait for future treatments.
Animal studies like this usually take years before they lead to human trials, and many treatments that work in animals never prove useful in people. If future human studies are launched, it could take several more years to learn whether relaxin is safe and effective. Patients should not expect any new relaxin-based treatment for heart failure in the near term.
Frequently Asked Questions
Does relaxin-2 help with heart failure with preserved ejection fraction?
A 2026 rat study found that synthetic relaxin-2 improved stiff-heart function and reduced left atrium size after two weeks. Human research is still needed, so this finding should not be used as a treatment guide for people.
What is heart failure with preserved ejection fraction?
Heart failure with preserved ejection fraction is a condition where the heart muscle pumps normally but becomes stiff and struggles to fill with blood. It often causes breathlessness, fatigue, and swelling, and current treatments mainly relieve symptoms.
Can a high-fat diet cause heart failure in rats?
In the 2026 study, rats of a special strain fed a high-fat diet developed heart stiffness, enlarged left atrium, and higher blood sugar and blood pressure over 11 weeks. The findings describe this model in animals and do not directly show the same effect in people.
Is relaxin a safe treatment for heart problems?
Relaxin has been tested in human trials for acute heart failure, with mixed results, and it is not a standard treatment today. Safety and effectiveness for long-term heart failure are not yet established, so patients should only use it within a doctor-supervised research setting.
Want to Apply This Research?
- Log your resting heart rate each morning before getting out of bed, and record your home blood pressure at least three times per week. Also note any shortness of breath during daily activities on a simple 1 to 5 scale. Sharing these trends with your doctor can help track heart health over time.
- Focus on habits that support heart health, such as limiting highly processed, high-fat foods, walking for 20 to 30 minutes most days if your doctor approves, and taking prescribed medications on schedule. Use the app to set reminders for these habits and to check off completed goals each day.
- Track heart-related measures weekly and review monthly trends in the app, such as blood pressure, resting heart rate, weight, and symptom scores. Share a summary report with your healthcare provider at each visit. If you notice sudden changes like fainting, chest pain, or a racing heartbeat that does not settle, seek medical care right away rather than relying on app data.
This article summarizes an early animal study in rats and has not been tested in humans. It is for general education only and is not medical advice. Do not start, stop, or change any heart medication or treatment based on this research. Talk with a qualified healthcare provider, such as a cardiologist, about any heart symptoms or treatment questions.
This research translation is published by Gram Research, the science division of Gram, an AI-powered nutrition tracking app.