Researchers have discovered that an anti-aging gene can reverse the biological age of the heart by 10 years. The healthy mutant gene, found in many centenarians, has been shown to protect the heart against diseases associated with aging, such as heart failure. The researchers found that a single administration of the gene halted the decay of heart function in middle-aged mice and rewound the heart’s biological clock age by more than 10 years in elderly mice. The findings offer a potential target for patients with heart failure.

The gene in question is known as TGF-beta receptor type 1 (TGFBR1). It is part of the TGF-beta signaling pathway, which regulates cell growth and division, as well as cell differentiation and migration. This pathway is important for many physiological processes, including embryonic development, wound healing, and immune system function.

In recent years, researchers have discovered that mutations in the TGFBR1 gene are associated with increased lifespan and improved healthspan in several species, including humans. Centenarians and their offspring are more likely to carry these mutations, suggesting that they play a role in exceptional longevity.

The new study builds on previous research that showed that TGFBR1 mutations can protect against cardiovascular disease by promoting the growth of new blood vessels and reducing inflammation. In the current study, the researchers found that a single injection of the mutant TGFBR1 gene can improve heart function in middle-aged and elderly mice. They found that the gene therapy prevented further deterioration of heart function and improved the mice’s ability to exercise. In fact, the treated mice had similar heart function to healthy, untreated mice.

In a second test, they found that the gene therapy improved the mice’s heart function and reversed some of the age-related changes in their hearts. Specifically, the treated mice had increased cardiac output, reduced heart weight, and improved capillary density, all of which are markers of improved heart function.

The researchers also tested the gene therapy approach in human cardiac cells in a lab. They collected heart cells from elderly patients with severe heart problems, including those requiring heart transplantation, and compared their function to healthy individuals. They found that adding the mutant TGFBR1 gene/protein to the heart cells improved their function and efficiency in building new blood vessels.

While the results are promising, the researchers caution that more research is needed to determine the safety and efficacy of this approach in humans. They are currently planning clinical trials to test the therapy in patients with heart failure.

The researchers also note that this gene therapy approach may have broader applications beyond heart failure. TGF-beta signaling is important for many physiological processes, including immune system function, wound healing, and cancer development. Therefore, the mutant TGFBR1 gene may have therapeutic potential for other age-related diseases.

In summary, the discovery of a gene associated with exceptional longevity has led to the development of a gene therapy approach that can improve heart function and reverse age-related changes in the heart. The therapy may have potential applications for patients with other age-related diseases, as well. In short, we could soon be able to set the clock back 10 years on our heart health.