Therapeutic Target To Reverse Muscle Wasting in Aging Identified

MedicalResearch.com Interview with: Dr. David Sebastián IRB Barcelona and CIBERDEM researcher

Dr. David Sebastián

MedicalResearch.com Interview with:
Dr. David Sebastián
IRB Barcelona and CIBERDEM researcher

MedicalResearch.com: What is the background for this study? What are the main findings?

Response: 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. However, the underlying causes of sarcopenia are unknown and thus no treatment is available for this condition.

Importantly, we have found that the mitochondrial protein Mitofusin 2 is required to preserve healthy muscles in mice. Mitofusin 2 is a mitochondrial protein involved in ensuring the correct function of mitochondria, and it has several activities related to autophagy, a crucial process for the removal of damaged mitochondria. The loss of Mitofusin 2 impedes the correct function of mitochondrial recycling and consequently damaged mitochondria accumulate in muscle cells.

MedicalResearch.com: What should readers take away from your report?

Response: Sarcopenia is a major health issue, because it is a very important factor in the frailty syndrome, which impedes some elderly people from going about their everyday lives. Therefore, our finding stablish Mitofusin 2 as a possible therapeutic target to combat sarcopenia and frailty.

MedicalResearch.com: What recommendations do you have for future research as a result of this study?

Response: Thanks to this study, we have also identified and described an autophagy rescue system which kicks in regardless of Mitofusin 2 levels and allows cells to partially recover the mitochondrial recycling system in skeletal muscle. Boost of this alternative or other mechanisms oriented to increase skeletal muscle autophagy and to maintain a healthier mitochondrial system would be vital to maintain muscle fitness during age.

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Citation:
David Sebastián, Eleonora Sorianello, Jessica Segalés, Andrea Irazoki, Vanessa Ruiz-Bonilla, David Sala, Evarist Planet, Antoni Berenguer-Llergo, Juan Pablo Muñoz, Manuela Sánchez-Feutrie, Natàlia Plana, María Isabel Hernández-Álvarez, Antonio L. Serrano, Manuel Palacín, and Antonio Zorzano. Mfn2 deficiency links age-related sarcopenia and impaired autophagy to activation of an adaptive mitophagy pathway. The EMBO Journal, June 2016 DOI: 10.15252/embj.201593084

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