Cardiac stress, for example a heart attack or high blood pressure, frequently leads to pathological heart growth and subsequently to heart failure. Two tiny RNA molecules play a key role in this detrimental development in mice, as researchers at the Hannover Medical School and the Göttingen Max Planck Institute for Biophysical Chemistry have now discovered.
When they inhibited one of those two specific molecules, they were able to protect the rodent against pathological heart growth and failure. With these findings, the scientists hope to be able to develop therapeutic approaches that can protect humans against heart failure.
Respiratory distress, fatigue, and attenuated performance are symptoms that can accompany heart failure. Germany-wide approximately 1.8 million people suffer from this disease. A reason for this can be an enlarged heart, a so-called cardiac hypertrophy. It may develop when the heart is subjected to permanent stress, for example, due to persistent high blood pressure or a valvular heart defect. In order to boost the pumping performance, the heart muscle cells enlarge – a condition that frequently results in heart failure if not treated.
A research team at the Göttingen Max Planck Institute for Biophysical Chemistry and the Hannover Medical School discovered that two small RNA molecules play a key role in the growth of heart muscle cells: the microRNAs miR-212 and miR-132.
The scientists had observed that these microRNAs are more prevalent in the cardiac muscle cells of mice suffering from cardiac hypertrophy. To determine the role that the two microRNAs play, the scientists bred genetically modified mice that had an abnormally large number of these molecules in their heart muscle cells.
"These rodents developed cardiac hypertrophy and lived for only three to six months, whereas their healthy conspecifics had a normal healthy life-span of several years," explained Kamal Chowdhury, researcher in the department of molecular cell biology at the Max Planck Institute for Biophysical Chemistry.