The pathological atrophy of skeletal muscle is a serious biomedical problem for which no effective treatment is currently available. Those most affected populations are the elderly diagnosed with sarcopenia and patients with cancer, AIDS, and other infectious diseases that develop cachexia. A study by scientists at the Institute for Research in Biomedicine (IRB), in Barcelona, headed by Antonio Zorzano, professor from the Department of Biochemistry and Molecular Biology at the University of Barcelona (UB), reveals a potential therapeutic target to tackle muscle wasting in these risk populations.

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The study is published in the Journal of Clinical Investigation (JCI), one of the journals with highest impact in experimental medicine. Researchers associate the activity of the DOR protein with muscle atrophy and point to DOR as a plausible target against which to develop a drug to prevent muscle deterioration in certain diseases. The article is also signed by researchers Xavier Testar and Manuel Palacín, from the Department of Biochemistry and Molecular Biology of UB, among other experts.

DOR (Diabetes and Obesity Regulated), also known as TP53INP2, is a protein involved in autophagy, a quality control process that ensures cells stay healthy. The researchers have found that increased DOR expression in the muscle of diabetic mice leads to enhanced autophagy, which in turn favours the loss of muscle mass in these animals.

The advantage of developing a DOR inhibitor is that autophagy, a process necessary to keep cells healthy, would not be completely blocked in the absence of this protein. DOR is not essential for autophagy, but acts more as an accelerator. Thus, the inhibition of DOR would only partially reduce autophagy as other molecules involved would exert their activity normally, thus maintaining the levels.

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