A new drug target to treat and prevent the progression of heart failure has been identified by researchers at Mount Sinai School of Medicine.
The team evaluated failing human and pig hearts and discovered that SUMO1, a so-called "chaperone" protein that regulates the activity of key transporter genes, was decreased in failing hearts.
When the researchers injected SUMO1 into these hearts via gene therapy, cardiac function was significantly improved.
This research indicates that SUMO1 may play a critical role in the pathogenesis of heart failure.
"Our experiments over the last four years beginning with the discovery of SUMO1 as an interacting protein of SERCA2a have shown that it plays a critical role in the development of heart failure," said lead researcher Roger J. Hajjar, MD, Director of Mount Sinai's Wiener Family Cardiovascular Research Laboratories.
"In fact, SUMO1 may be a therapeutic target at the earliest signs of development, and may be beneficial in preventing its progression, a much-needed advance for the millions suffering from this disease."
The study has been published online in Nature.