Researchers at Johns Hopkins, UC San Diego, and other institutions have identified a “fountain of youth” for the heart – a protein that helps keep heart muscle healthy as it ages, which could eventually lead to treatments for age-related heart failure.

The protein, called vinculin, increases over time, altering the shape and performance of cardiac muscle cells. Noting that in the human heart, there is little cell turnover or regeneration, the researchers looked at the cardiac proteomes of fruit flies, rats, and monkeys to identify molecular alterations that help sustain the aging heart.

“We observed that this protein was increasing,” Anthony Cammarato, co-principal investigator on the study and an assistant professor of medicine and physiology at the Johns Hopkins University School of Medicine, told DOTmed News. “We thought it was going to be deleterious, but it was actually beneficial.”
The research, published June 17 in the journal “Science Translational Medicine,” found that cardiac-specific vinculin overexpression increased the median life span of fruit flies by more than 150 percent.

The researchers looked at different strains of fruit flies, including one that is naturally deficient in vinculin, altering the genes in those flies to produce more of the protein. They then found that the hearts of flies with normal vinculin genes, and the hearts of the genetically altered flies, tolerated stress much better than the hearts of the vinculin-deficient flies.

The effects of the protein would have to be studied further in mammals that are more similar to humans, but therapies to enhance the molecular mechanisms already in place, such as gene therapies to get the protein to overexpress, could slow down the decline in function in the hearts of aging patients.

“With regard to clinical application, our data suggest that vinculin overexpression alone may be sufficient to improve cardiac outcome during aging, indicating that intervention with vinculin mRNA may be a viable therapy,” the study authors wrote. “Application of vinculin-based gene therapies in preclinical models should be explored for their potential to prevent or delay age-related dysfunction.”

Cammarato said that while it's inevitable that the performance of the heart is going to decline naturally, therapies could help patients affected by heart failure, which is estimated to affect more than 8 million people in the United States over the next decade.

“If we can help sustain cardiac performance, we might not be able to improve life span but maybe health span,” Cammarato said.

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