Japanese researchers have identified a receptor protein on the surface of heart cells that promotes chronic heart failure, affecting more than 20 million people worldwide.
Japanese researchers have identified a receptor protein on the surface of heart cells that promotes chronic heart failure, affecting more than 20 million people worldwide.
The study also suggests that inhibiting this protein called corticotropin could help treat a disease.
Chronic heart failure is caused by a variety of conditions that damage the heart, including coronary heart disease, hypertension, and diabetes.
Lead researcher Mikito Takefuji from Nagoya University in the New York discovered that a signaling 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.
Sustained treatment of otherwise healthy mice with Ucn2 was sufficient to reduce cardiac function.
They found that the activation of Crhr2 by Ucn2 stimulates several downstream signaling pathways that result in the expression of genes that impair heart function.
Mice lacking Crhr2 were protected from the effects of Ucn2 and were resistant to developing heart failure. A small molecule that inhibits Crhr2 was similarly effective in maintaining cardiac function after damage to the heart.
Takefuji further stated that constitutive Crhr2 activation causes cardiac dysfunction and that Crhr2 blockade could be a promising therapeutic strategy for patients with chronic heart failure.
The study published in the journal of Experimental Medicine.
(This article has not been edited by DNA's editorial team and is auto-generated from an agency feed.)
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