Professor Mathias Gautel

BHF Chair of Molecular Cardiology

Professor Gautel's team is deciphering how heart muscle cells work to enable the heart to pump. Their research sheds light on understanding heart muscle diseases and how they might be prevented, treated, or cured.

Professor Gautel is based at the Cardiovascular Division and Randall Division of Cell and Molecular Biophysics - part of the BHF Centre for Research Excellence at King's College, London.

Cardiomyopathy and heart failure

Cardiomyopathies are diseases of the heart muscle where the heart is abnormally enlarged or the walls are thickened. As a result the heart can become weak and struggle to pump normally. When the heart is struggling to pump, people can have heart failure.

Professor Gautel's team is discovering how specialised proteins work together to create the powerful muscular contractions in heart cells, using state-of-the-art technology. This work is helping to unravel the mechanisms that lead to heart muscle conditions.

Molecular machinery of the heart

Many hereditary diseases of the heart muscle are linked to malfunctions in the proteins that link together to cause muscle contraction. These repetitive arrangements of proteins are called sarcomeres.

If sarcomeres are not formed properly, the heart responds inadequately and can eventually fail. This can happen because of hereditary conditions such as cardiomypathy as well as other factors such as high blood pressure.

Sarcomeres generate force and movement. They are made up of three systems of muscle fibres: actin, myosin and titin. Sarcomeres are broken down and made anew depending on the body's demand on the heart.

Titin is the largest protein in the human body. It links actin and myosin filaments together. It senses changes to mechanical strain on the heart cells, as well as seeming to organise sarcomere turnover in response to the heart's workload.

A major focus for Professor Gautel's research is to understand the intricate details of how titin works in sarcomeres. Sarcomeres are not only part of a machine - they are a communication device. Their malfunction is critically involved in cardiomyopathies and heart failure.