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Protein protects the heart from cardiac hypertrophy

Dr. Derk Frank, a scientist from Heidelberg, was awarded the 2008 Gotthard Schettler Prize for Cardiovascular Research.

There is a protein produced by the human body that protects the heart from damage caused by high blood pressure. The scientist Dr. Derk Frank from Heidelberg has discovered that calsarcin 1 protects the heart against pathological alterations caused by overstraining. Last month, Frank was awarded the 2008 Gotthard Schettler Prize for Cardiovascular Research for his achievements, which had previously been published in the journal “Circulation”.
Dr. Derk Frank, Department of Cardiology at the Medical Clinic of the University of Heidelberg (Foto: University Hospital Heidelberg)
The award comes with a purse of 10,000 euros and is named after the well-known cardiologist Gotthard Schettler, director of the Medical Clinic of the University of Heidelberg from 1963 to 1986. Dr. Derk Frank shares the award with Dr. Dietmar Trenk from the Heart Centre in Bad Krozingen.

Permanent high blood pressure and constricted openings in the cardiac valve or aorta mean hard work for the heart which tends to compensate in a way that leads to cardiac hypertrophy. The situation eventually impairs the heart’s pumping capacity and can result in cardiac arrhythmia or even heart failure. Additional risk factors are weight and age: more than 40 per cent of all people over 70 suffer from cardiac hypertrophy.

Calsarcin 1 protects the heart from excessive muscle growth

Calsarcin 1 (CS1) plays an important role in this disease mechanism. The protein was identified and characterised in 2000 by a group of researchers led by Dr. Norbert Frey, senior physician in the Department of Cardiology, Angiology and Pneumology (Director: Prof. Dr. med. H.A. Katus) at the Medical Clinic of the University of Heidelberg: the protein is only present in the cells of the heart muscle and prevents the calcineurin signalling pathway from causing cardiac hypertrophy. Genetically engineered mice that are unable to produce CS1 develop more severe hypertrophy under conditions of hypertension.

“We have now investigated the issue from the opposite angle: Are cells that produce elevated levels of CS1 less prone to hypertrophy-inducing stimuli?” said Dr. Derk Fank, assistant doctor in the Department of Cardiology, Angiology and Pneumology and first author of the paper published in “Circulation”. Experiments on isolated heart muscle cells from rats showed that signalling pathways that generate excessive muscle growth are not activated when there are high levels of CS1 present. Mice that were genetically engineered to produce more CS1 than unmodified mice did not develop hypertrophy when subjected to long-term infusion of the tissue hormone angiotensin II that leads to an increase in blood pressure and has a direct effect on the heart muscle. “Both CS1 mice and wild-type mice developed arterial hypertension, but in contrast to wild-type mice, animals treated with angiotensin II did not display cardiac hypertrophy,” said Dr. Frank.

Promising approach for future cardiac hypertrophy therapy

Cardiac hypertrophy is a high risk factor for further cardiac diseases and sudden heart failure. Calsarcin-1 is a natural inhibitor that interrupts the mechanism of this disease in the heart cells. Thus, the overexpression of CS1 could represent a novel approach for the future treatment of cardiac hypertrophy.

Literature:
Frank D, Kuhn C, van Eickels M, Gehring D, Hanselmann C, Lippl S, Will R, Katus HA, Frey N: Calsarcin-1 protects against angiotensin-II induced cardiac hypertrophy. Circulation. 2007;116(22):2587-2596


Source: University Hospital Heidelberg press release - 14 Oct. 2008

Further information:
Dr. Derk Frank
Department of Cardiology, Angiology and Pneumology
Medical Hospital
University of Heidelberg
Tel.: +49 (0)6221-56 398 30
E-mail: derk.frank@med.uni-heidelberg.de

Website address: https://www.gesundheitsindustrie-bw.de/en/article/news/protein-protects-the-heart-from-cardiac-hypertrophy