Why do people with heart disease develop muscle weakness?

MicroRNAs, GDF-15 and myostatin regulate skeletal muscle mass in chronic heart failure and pulmonary arterial hypertension

Paul Kemp (lead researcher)

Imperial College London

Start date: 26 January 2015 (Duration 3 years)

People with severe heart failure can develop muscle wasting and weakness, which makes it difficult to perform everyday tasks or exercise. Muscle wasting also occurs in people with pulmonary arterial hypertension, a condition where high blood pressure in the arteries that carry blood from the heart to the lungs causes severe breathing difficulties and heart failure. Understanding what causes muscle weakness may reveal targets for new treatments to restore muscle mass and, ultimately, quality of life. Dr Paul Kemp and his team at Imperial College London are studying small molecules that control the way our genes are expressed, called microRNAs. They have found that certain microRNAs make muscle cells more sensitive to a protein called myostatin, which causes muscles to break down. They also found that some people have specific patterns of microRNAs that make them more susceptible to muscle wasting, because they do not repair their muscles effectively. Dr Kemp has now been awarded a PhD studentship to allow a young researcher to investigate microRNAs in more detail. The student will establish if rats and humans with heart failure and pulmonary hypertension have similar changes in their skeletal muscle microRNAs that increase sensitivity to myostatin. They will also find out if heart failure patients with the most depleted skeletal muscle have the same microRNA profile that is associated with poor repair. This research will reveal new ways to sustain or boost muscle mass using drugs, which would ultimately improve the quality of life for people with heart failure and other conditions.

Project details

Grant amount £122,878
Grant type Fellowship
Application type PhD Studentship
Start Date 26 January 2015
Duration 3 years
Reference FS/14/71/31038
Status Complete

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