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Slowing down muscle loss in heart failure patients

New molecular signaling path deciphered

August 10, 2015
Charité - Universitätsmedizin Berlin
Whenever cardiac insufficiency or serious heart defects worsen, such deterioration is often associated with a loss of muscular mass and muscular strength. Scientists have now succeeded in identifying the mechanism that underlies this disease, also known as cardiac cachexia. On the basis of these latest findings it may now be possible to influence the processes that strengthen and accelerate protein degradation in the body with the help of certain medications.

Patients in advanced states of myocardial insufficiency generally lose their muscle mass and muscle strength. Indeed a fact that until now has negatively impacted the clinical course of the disease and that has resulted in poor prognoses for patients. Such pathological muscle loss impacts the skeletal muscles in particular. The responsible molecular signaling pathways have not yet been fully understood. One cause of this degenerative process lies in the system that regulates the blood pressure and salt/water supply in the body -- the so-called renin-angiotensin-aldosterone system (RAAS). This is strongly activated in the context of the disease process and associated with cardiac cachexia leading to an increase in the formation of the effector peptide angiotensin II. Angiotensin II directly affects the muscle and increases protein degradation there, resulting in a loss of muscular mass and strength.

To date, patients suffering from heart failure have been treated with medications that inhibit the renin-angiotensin-aldosterone system. While this treatment option slows muscle loss for a certain period, conventional medications lose their efficacy after just a few years. With a view to finding new treatment methods, scientists collaborating with Dr. Jens Fielitz, Cardiologist at the Charité and Group Leader at the Experimental and Clinical Research Center (ECRC) have now been examining the precise signal pathway that prompts protein degradation in muscle. In particular, angiotensin II increases the production of a specific protein in muscle called muscle RING-finger 1 (MuRF1), which plays a key role in muscle loss.

"We have been able to identify and characterize the function of a new transcription factor that regulates this process. Our experiments have also revealed the specific mechanisms that either activate or inhibit the production of MuRF1 protein, that is to say that either reduce or increase muscle loss," says Privatdozent Dr. Jens Fielitz. He adds "Our findings can now provide insights into important unanswered questions in that they delineate a new signal pathway that is important in the emergence of cardiac cachexia." By suppressing this signal it may be possible to inhibit the muscle loss caused by angiotensin II and therefore offers high potential in terms of therapeutic options.

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Materials provided by Charité - Universitätsmedizin Berlin. Note: Content may be edited for style and length.

Journal Reference:

  1. Song, Sibylle Schmidt, Rhonda Bassel-Duby, Eric N. Olson, Jens Fielitz. Angiotensin II Induces Skeletal Muscle Atrophy by Activating TFEB-Mediated MuRF1 Expression. Circulation Research, June 2015 DOI: 10.1161/CIRCRESAHA.114.305393

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Charité - Universitätsmedizin Berlin. "Slowing down muscle loss in heart failure patients: New molecular signaling path deciphered." ScienceDaily. ScienceDaily, 10 August 2015. <>.
Charité - Universitätsmedizin Berlin. (2015, August 10). Slowing down muscle loss in heart failure patients: New molecular signaling path deciphered. ScienceDaily. Retrieved May 23, 2017 from
Charité - Universitätsmedizin Berlin. "Slowing down muscle loss in heart failure patients: New molecular signaling path deciphered." ScienceDaily. (accessed May 23, 2017).