3 days popular7 days popular1 month popular3 months popular

The absence of a single protein spurs muscle aging in mice

One of the alterations that most affects the quality of life of the elderly is muscle wastage and the resulting loss of strength, a condition known as sarcopenia. At about 55 years old, people begin to lose muscle mass, this loss continues into old age, at which point it becomes critical. The underlying causes of sarcopenia are unknown and thus no treatment is available for this condition. A study at the Institute for Research in Biomedicine (IRB Barcelona) done in collaboration with the University of Barcelona (UB) and the CIBER’s area of Diabetes and Associated Metabolic Diseases (CIBERDEM) has discovered that Mitofusin 2 is required to preserve healthy muscles in mice. In the paper, which has been published in The EMBO Journal, these researchers indicate that this protein could serve as a therapeutic target to ameliorate sarcopenia in the elderly.

Headed by Antonio Zorzano, coordinator of the Molecular Medicine Programme at IRB Barcelona, and UB and ICREA Academia professor, the scientists observed that during aging mice specifically lose the expression of Mitofusin 2 in muscle. They demonstrate that low activity of this protein in 24-month old mice (the equivalent of a person aged 80) is directly associated with muscle wastage and the sarcopenia observed. The scientists confirm the link between the loss of Mitofusin 2 and muscle aging when the expression of the protein is suppressed in the muscles of 6-month-old animals (equivalent to a person of 30) as these animals showed accelerated aging, reproducing thus muscle conditions of aged mice.

Muscle mitochondrion
On the left, a normal muscle mitochondrion. On the right, a mitochondrion in Mitofusin 2-deficient muscle
Image Credit: D. Sebastian, IRB Barcelona, CIBERDEM