Research from the Icahn School of Medicine at Mount Sinai in New York has identified a protein, called CCN5, which can reverse established cardiac fibrosis in heart failure, which accounts for roughly 450,000 deaths each year in the United States.
A research team, led by Roger J. Hajjar, MD, professor of medicine and director of the cardiovascular research center at the Icahn School of Medicine, evaluated the effect CCN5 had on reversing cardiac fibrosis in experimental animal models. They induced extensive cardiac fibrosis in the animals with heart failure, and then proceeded to transfer CCN5 to the hearts. Eight weeks later, the team examined the cellular and molecular results.
The findings revealed CCN5 reversed cardiac fibrosis in the models.
"Our research is the first to demonstrate the ability to reverse cardiac fibrosis in heart failure models by targeting a specific gene," said Dr. Hajjar. "These findings demonstrate that CCN5 may provide a novel platform for the development of targeted anti-cardiac fibrosis therapies, which could benefit many patients with previously untreatable heart failure."
The therapeutic efficacy of CCN5 continues to be investigated in pre-clinical models of heart failure with extensive fibrosis.
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