They discover a new way to combat muscle loss with aging

David Sebastian, Antonio Zorsano and Marc Beltra, CIBERDEM researchers, at IRB Barcelona

CYBER | Monday, April 22, 2024

Sarcopenia is a common disease in older people, which is characterized by the progressive loss of muscle mass and function, which can significantly reduce your quality of life and increase your risk of falls, injuries and addiction. Research into this phenomenon is important for developing effective strategies that will allow populations to age healthy and independent.

A study led by Antonio Zorzano from IRB Barcelona, ​​and David Sebastiannow professor at the University of Barcelona (UB), published in the journal Autophagy, demonstrates that a protein called TP53INP2 may play a key role in the fight against sarcopenia. The work, developed in collaboration with Sant Joan de Déu Hospital in Sant Boi, shows that high levels of TP53INP2 in muscle are associated with greater muscle strength and healthier aging in humans.

Loss of muscle mass usually begins after age 55 and negatively impacts the functionality and health of older adults. Sarcopenia results in increased weakness, physical disability, and the need for long-term care. Through an exhaustive study, the scientific team discovered the decisive role of the TP53INP2 protein, It regulates autophagy, a cellular process essential for removing damaged proteins and organelles and maintaining muscle mass and function.

Through experiments in mouse models and analysis of human muscle tissue samples, the researchers found that TP53INP2 levels decline with age. However, artificially increase the amount of this protein in the muscles, either long-term exposure to young mice or temporary exposure to older mice using genetic engineering techniques resulted in significant improvements in muscle mass and function.

These results suggest that increasing TP53INP2 activity and hence autophagy in muscle may be an effective strategy to combat sarcopenia and promote more active and healthy aging. In human studies, high levels of TP53INP2 were associated with greater strength and better physical performance, highlighting its potential as an indicator of healthy aging.

“This study not only highlights the importance of maintaining autophagy activity in muscle to prevent muscle loss, but also gives us hope for possible treatments that could improve or at least mitigate the effects of aging in our muscles.”explains Dr. Zorzanowho is also a professor in the Department of Biology at UB and a member of CIBERDEM. “In addition, activation of autophagy through TP53INP2 improved the quality of mitochondria, an important organelle in energy production, a process that we have shown in previous studies to be altered during aging.” emphasizes Dr. SebastianProfessor of the Department of Biochemistry and Physiology, Faculty of Pharmacy and Food Sciences, UB.

The collaboration with the Sant Joan de Déu Hospital was essential in providing access to biological samples from well-studied patients, allowing us to determine the association between muscle TP53INP2 expression and healthy aging in humans. This advance not only opens new avenues for research in the field of aging, but also suggests possible interventions that can significantly improve the quality of life of older adults, helping them maintain their independence and vitality.

Going forward, the research team will continue to study whether genetic factors, physical activity, or other habits such as diet play a determining role in each person’s TP53INP2 levels.

This work was made possible thanks to funding from the Ministry of Science, Innovation and Universities, the Generalitat of Catalonia and the Carlos III Institute of Health.

Link to the product:

TP53INP2-dependent activation of muscle autophagy reduces sarcopenia and promotes healthy aging.

David Sebastian, Marc Beltra, Andrea Irazoqui, David Sala, Pilar Aparicio, Cecilia Aris, Esmail Alibakhshi, Maria Rubio-Valera, Manuel Palacin, Juan Castellanos, Luis Lores and Antonio Zorsano

Autophagy (2024) DOI: 10.1080/15548627.2024.2333717

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