Article Sidebar
Main Article Content
Abstract
Background: Brain-derived neurotrophic factor (BDNF), a neurotrophin crucial for neuronal survival and differentiation, has emerged as a potential key player in sarcopenia development. This meta-analysis aimed to systematically evaluate the molecular mechanisms by which BDNF contributes to sarcopenia.
Methods: A comprehensive search of PubMed, Scopus, and Web of Science databases was conducted for studies published between 2018 and 2024 investigating the relationship between BDNF and sarcopenia at a molecular level. Studies were included if they met the following criteria: (1) examined BDNF signaling pathways in skeletal muscle; (2) assessed the impact of BDNF on muscle protein synthesis/degradation; (3) explored the role of BDNF in mitochondrial function and oxidative stress in muscle; and (4) investigated the influence of BDNF on muscle fiber type and neuromuscular junction integrity.
Results: A total of 28 studies (n = 1,245 participants) met the inclusion criteria. The meta-analysis revealed that lower BDNF levels were significantly associated with: reduced muscle protein synthesis (SMD = -0.85, 95% CI: -1.12 to -0.58, p < 0.001); increased muscle protein degradation (SMD = 0.62, 95% CI: 0.35 to 0.89, p < 0.001); impaired mitochondrial function (SMD = -0.71, 95% CI: -0.98 to -0.44, p < 0.001); increased oxidative stress (SMD = 0.55, 95% CI: 0.28 to 0.82, p < 0.001); a shift towards fast-twitch muscle fibers (SMD = 0.48, 95% CI: 0.21 to 0.75, p = 0.001); and compromised neuromuscular junction integrity (SMD = -0.92, 95% CI: -1.21 to -0.63, p < 0.001).
Conclusion: This meta-analysis provides compelling evidence that BDNF plays a pivotal role in the pathogenesis of sarcopenia through its multifaceted effects on muscle protein metabolism, mitochondrial function, oxidative stress, fiber type composition, and neuromuscular junction integrity.
Keywords
Article Details
As our aim is to disseminate original research article, hence the publishing right is a necessary one. The publishing right is needed in order to reach the agreement between the author and publisher. As the journal is fully open access, the authors will sign an exclusive license agreement.
The authors have the right to:
- Share their article in the same ways permitted to third parties under the relevant user license.
- Retain copyright, patent, trademark and other intellectual property rights including research data.
- Proper attribution and credit for the published work.
For the open access article, the publisher is granted to the following right.
- The non-exclusive right to publish the article and grant right to others.
- For the published article, the publisher applied for the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License.
