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Review
. 2025 Mar 1.
doi: 10.1007/s12033-025-01373-0. Online ahead of print.

The Roles of myomiRs in the Pathogenesis of Sarcopenia: From Literature to In Silico Analysis

Huanxia Jia #  1 , Nurgulsim Kaster #  2   3 , Rajwali Khan  4   5 , Amel Ayari-Akkari  6
Affiliations
Review

The Roles of myomiRs in the Pathogenesis of Sarcopenia: From Literature to In Silico Analysis

Huanxia Jia et al. Mol Biotechnol. .

Abstract

Senile sarcopenia is a condition of age-associated muscular disorder and is a significant health issue around the world. In the current review, we curated the information from the NCBI, PubMed, and Google Scholar literature and explored the non-genetic and genetic causes of senile sarcopenia. Interestingly, the myomiRs such as miR-1, miR-206, miR-133a, miR-133b, miR-208b, and miR-499 are skeletal muscle's critical structural and functional regulators. However, very scattered information is available regarding the roles of myomiRs in different skeletal muscle phenotypes through a diverse list of known target genes. Therefore, these pieces of information must be organized to focus on the conserved target genes and comparable effects of the myomiRs in regulating senile sarcopenia. Hence, in the present review, the roles of pathogenetic factors in regulating senile sarcopenia were highlighted. The literature was further curated for the roles of myomiRs such as hsa-miR-1-3p/206, hsa-miR-27-3p, hsa-miR-146-5p, and hsa-miR-499-5p and their target genes. Additionally, we used different bioinformatics tools and predicted target genes of the myomiRs and found the most critical target genes, shared pathways, and their standard functions in regulating muscle structure and functions. The information gathered in the current review will help the researchers to explore their possible therapeutic potential, especially the use of the myomiRs for the treatment of senile sarcopenia.

Keywords: Causes of sarcopenia; MiRNAs in sarcopenia; Muscular atrophy; MyomiRs; Sarcopenia.

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Conflict of interest statement

Declarations. Conflict of interest: The authors declare no conflict of interest.

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