Sarcopenia, a prevalent condition among the elderly, is characterized by a progressive decline in muscle mass and function, which can significantly diminish quality of life and increase the risk of falls, injuries, and dependency. More research is needed to create effective strategies that enable the aging population to remain healthy and independent. Now researchers from IRB Barcelona report that a protein may be the key to combatting sarcopenia.

The findings are published in Authophagy in an article titled, “TP53INP2-dependent activation of muscle autophagy ameliorates sarcopenia and promotes healthy aging,” and led by Antonio Zorzano, PhD, from IRB Barcelona, and David Sebastián, PhD, now a professor at the University of Barcelona (UB), in partnership with Parc Sanitari Sant Joan de Déu.

The new study demonstrates that increased levels of a protein named TP53INP2 in muscle correlate with greater muscular strength and healthier aging in humans.

Loss of muscle mass typically starts around the age of 55, and it has a detrimental effect on people’s ability to perform daily tasks and on their health. Conducting experiments on mouse models and analyzing human muscle tissue samples, the researchers observed a decrease in TP53INP2 levels with age. However, artificially boosting the presence of this protein in muscles—whether continuously in young mice or temporarily in older mice through genetic engineering techniques—led to a significant improvement in both muscle mass and function.

These findings suggest that promoting the activity of TP53INP2 and, consequently, autophagy in the muscle, could be an effective strategy to tackle sarcopenia, thereby contributing to a more active and healthier aging process.

“This study not only underscores the importance of keeping autophagy active in muscles to prevent muscle mass loss but also gives us hope regarding potential treatments that could improve the condition or at least mitigate the effects of aging on our muscles,” explained Zorzano, who is also a professor at the Faculty of Biology at UB and a member of CIBERDEM. “Furthermore, the activation of autophagy through TP53INP2 improved the quality of mitochondria, essential organelles in energy generation—a process that we had previously shown to be disrupted during aging,” highlighted Sebastián, a professor in the department of biochemistry and physiology at the Faculty of Pharmacy and Food Sciences of UB.

Moving forward, the researchers will continue to explore whether TP53INP2 levels in each person are influenced by genetic factors and physical activity, or, whether other habits, like nutrition, play a significant role.

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