New therapy can reduce muscle loss in patients with heart failure

Release date: 2015-08-13

In developed countries, patients with myocardial insufficiency are often associated with muscle loss and decreased muscle strength. In fact, until now, the negative impact on the clinical course of the disease can lead to poor patient prognosis. This pathological muscle loss particularly affects skeletal muscle growth. The molecular signaling pathway in this aspect is not fully understood at present. One reason for this degenerative process is the regulation of blood pressure and salt/water supply systems in the body, the so-called renin-angiotensin-aldosterone system (RAAS). This system is strongly activated in the context of the disease process and is associated with cardiogenic cachexia, resulting in increased formation of the effector peptide angiotensin II. Angiotensin II directly affects muscles and enhances protein degradation, resulting in muscle loss and decreased muscle strength.

To date, treatment of patients with heart failure with drugs has inhibited the renin-angiotensin-aldosterone system. Although this treatment slows muscle atrophy for a period of time, this traditional medicine loses its effectiveness only a few years later. In search of new treatments, scientists collaborated with Dr. Jens Fielitz, a Charité cardiologist and head of the Center for Experimental and Clinical Research (ECRC) who have tested the exact signaling pathways that suggest protein degradation in muscle. In particular, angiotensin II increases the production of specific proteins in the muscle called Muscle Ring Finger 1 (MuRF1), which plays a key role in muscle loss.

"We have been able to identify the function of a new transcription factor that regulates this process. Our experiments also revealed a specific mechanism that both activates and inhibits the production of MuRF1 protein, which means both reduction and increase. Muscle loss," said Dr. Privatdozent Jens Fielitz.

He added, "Our findings can provide a deep understanding of important and unresolved issues in which they portray a new signaling pathway that is important for the emergence of cardiogenic cachexia." By suppressing this signal It can inhibit muscle loss caused by angiotensin II, thus providing a very promising treatment.

Source: Bio Valley

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