Researchers in Japan have found a receptor protein on the surface of heart cells that promotes chronic heart failure.

The findings, published in The Journal of Experimental Medicine, suggests that inhibiting this protein could help treat a disease that affects more than 20 million people worldwide.

Chronic heart failure is caused by a variety of conditions that damage the heart, including coronary heart disease, hypertension and diabetes. 

Although the heart initially tries to compensate for this damage and maintain its function by, for example, growing larger, cardiac function gradually declines until the heart is no longer able to pump enough blood and oxygen around the body. 

A team of researchers led by Mikito Takefuji from Nagoya University School of Medicine discovered that a signalling protein called corticotropin releasing hormone receptor 2 (Crhr2) is expressed on the surface of heart muscle cells, or cardiomyocytes, and that Crhr2 levels increase in mice suffering from heart failure.

Crhr2 is a G protein-coupled receptor whose ability to alter cardiomyocyte function is activated by a protein called urocortin 2 (Ucn2). 

Ucn2 levels were elevated in the blood of both mice and human patients with chronic heart failure, the researchers found. 

"Our results suggest that constitutive Crhr2 activation causes cardiac dysfunction and that Crhr2 blockade could be a promising therapeutic strategy for patients with chronic heart failure," Takefuji said.