Sarcopenia, a common condition in older adults, is a gradual loss of muscle mass and function that significantly reduces quality of life and increases the risk of falls, injuries, and the need for care. A deeper understanding of this phenomenon is crucial to devise effective strategies to help older adults live healthy and independent lives.
A study co-led by Dr Antonio Zorzano of IRB Barcelona and Dr David Sebastián, now a professor at the University of Barcelona (UB), has revealed that a protein called TP53INP2 is crucial for preventing sarcopenia. The study, conducted in collaboration with Parc Sanitari Sant Joan de Déu, has shown that increased levels of this protein in muscle correlate with increased strength and healthy ageing in humans.
Loss of muscle mass typically begins around age 55 and negatively impacts health and the ability to perform daily tasks. Sarcopenia leads to increased frailty, disability and the need for long-term care.
By working with mouse models and analysing human muscle tissue samples, the researchers observed that TP53INP2 levels decline with age, but artificially increasing the presence of this protein in muscle, either continuously in young mice or temporarily through genetic engineering in older mice, significantly improved both muscle mass and function.
These findings suggest that promoting TP53INP2 activity, and therefore muscle autophagy, may be an effective strategy to tackle sarcopenia and contribute to a more active and healthy aging process. Human studies have shown that higher TP53INP2 levels are associated with increased muscle strength and improved physical performance, highlighting the protein’s potential as an indicator of healthy aging.
“This study not only highlights the importance of keeping autophagy active in muscles to prevent muscle mass loss, but also gives us hope about possible treatments that could improve the condition or at least reduce the effects of muscle ageing,” explains Dr. Zorsano, professor at the UB Department of Biology and member of CIBERDEM. “Furthermore, the activation of autophagy by TP53INP2 improved the quality of mitochondria, organelles essential for energy generation, a process that has previously been shown to be disrupted during ageing,” emphasizes Dr. Sebastian, professor at the Department of Biochemistry and Physiology at the UB Faculty of Pharmacy and Food Science.
The collaboration with Parc Sanitari Sant Joan de Déu was crucial, allowing access to biological samples from well-characterized patients, which enabled the researchers to establish a link between TP53INP2 muscle expression and healthy aging in humans. This advance not only paves the way for further research into aging, but also suggests interventions that could significantly improve the quality of life of older adults, helping them maintain their independence and vitality.
The researchers plan to continue investigating whether an individual’s TP53INP2 levels are influenced by genetic factors or physical activity, or whether other habits, such as nutrition, play an important role.
This research was made possible thanks to funding from the Ministry of Science, Innovation and Universities, the Catalan Government and the Carlos III Health Institute.
