Abstract

Background: Sarcopenia, the age-related decline in muscle mass and function, poses a significant public health challenge. Myostatin, a potent negative regulator of muscle growth, has emerged as a potential therapeutic target for sarcopenia. This meta-analysis aims to comprehensively assess the association between myostatin and sarcopenia, synthesizing evidence from human and animal studies. Methods: A systematic search of PubMed, Embase, and Cochrane Library was conducted to identify relevant studies published between 2018 and 2024. Studies investigating the relationship between myostatin levels or inhibition and sarcopenia-related outcomes were included. Data on myostatin levels, muscle mass, muscle strength, and physical function were extracted. Standardized mean differences (SMDs) and 95% confidence intervals (CIs) were calculated using random-effects models. Results: A total of 25 studies (15 human, 10 animal) met the inclusion criteria. The meta-analysis revealed a significant association between elevated myostatin levels and reduced muscle mass (SMD = -0.65, 95% CI: -0.82 to -0.48, p < 0.001). Myostatin inhibition was associated with increased muscle mass (SMD = 0.52, 95% CI: 0.35 to 0.69, p < 0.001) and improved muscle strength (SMD = 0.41, 95% CI: 0.23 to 0.59, p < 0.001). Conclusion: This meta-analysis provides compelling evidence for the involvement of myostatin in sarcopenia. Elevated myostatin levels are associated with decreased muscle mass, while myostatin inhibition appears to promote muscle growth and improve function. These findings highlight the potential of targeting myostatin as a therapeutic strategy for sarcopenia.

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.