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<p>Sarcopenia (SARC) presents considerable challenges to the quality of life for the elderly and exerts a significant economic strain on healthcare systems. Contemporary therapeutic methods, such as physical activity, dietary supplementation, and medication, frequently demonstrate restricted effectiveness and significant individual variation. This study seeks to identify new therapeutic targets through the analysis of lysosomal autophagy-related differentially expressed genes (LARDEGs) associated with SARC. Differentially expressed genes(DEGs) related to SARC were identified through an extensive analysis of microarray datasets (GSE8479 and GSE1428) obtained from the Gene Expression Omnibus. Gene Ontology, Kyoto Encyclopedia of Genes and Genomes pathway analysis, protein-protein interaction (PPI) network analysis, and Gene Set Enrichment Analysis were used to assess the biological functions, molecular pathways, autophagy-related molecular markers, and immune microenvironment linked to SARC DEGs. Our findings identified 12 LARDEGs, including <i>BHLHE41</i>,<i> HLTF</i>,<i> UBE2D1</i>,<i> UBE2D2</i>,<i> NPC1</i>,<i> NDRG1</i>,<i> SLC22A18</i>,<i> CDKN1A</i>,<i> CALCOCO2</i>,<i> SCARB2</i>,<i> LGALS1</i>,<i> and RPS27A</i>, that were significantly correlated with energy metabolism and mitochondrial function. We constructed a PPI network that identified six crucial hub genes: <i>BHLHE41</i>,<i> UBE2D1</i>,<i> UBE2D2</i>,<i> CDKN1A</i>,<i> SCARB2</i>,<i> and RPS27A</i>. This network provides significant insights into their functional roles and their potential as therapeutic targets. Additionally, an examination of immune infiltration demonstrated significant differences in the quantities of resting natural killer (NK) cells and M2 macrophages between SARC samples and control samples. <i>CDKN1A</i> displayed a positive correlation with M2 macrophages and an inverse relationship with resting NK cells. The results show how important the immune microenvironment is to the spread of SARC, suggesting promising pathways for the creation of immunotherapeutic strategies. Our research elucidates the molecular pathways implicated in SARC and establishes a foundation for future therapeutic approaches. However, additional validation is crucial to translating these findings into viable clinical applications.</p>

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Integrated transcriptomic analysis identifies lysosomal autophagy-related genes in sarcopenia

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年10月22日

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  • Ye Zhou,
  • Yue Qian,
  • Xin Yuan,
  • Qingqing Zhu

摘要

Sarcopenia (SARC) presents considerable challenges to the quality of life for the elderly and exerts a significant economic strain on healthcare systems. Contemporary therapeutic methods, such as physical activity, dietary supplementation, and medication, frequently demonstrate restricted effectiveness and significant individual variation. This study seeks to identify new therapeutic targets through the analysis of lysosomal autophagy-related differentially expressed genes (LARDEGs) associated with SARC. Differentially expressed genes(DEGs) related to SARC were identified through an extensive analysis of microarray datasets (GSE8479 and GSE1428) obtained from the Gene Expression Omnibus. Gene Ontology, Kyoto Encyclopedia of Genes and Genomes pathway analysis, protein-protein interaction (PPI) network analysis, and Gene Set Enrichment Analysis were used to assess the biological functions, molecular pathways, autophagy-related molecular markers, and immune microenvironment linked to SARC DEGs. Our findings identified 12 LARDEGs, including BHLHE41, HLTF, UBE2D1, UBE2D2, NPC1, NDRG1, SLC22A18, CDKN1A, CALCOCO2, SCARB2, LGALS1, and RPS27A, that were significantly correlated with energy metabolism and mitochondrial function. We constructed a PPI network that identified six crucial hub genes: BHLHE41, UBE2D1, UBE2D2, CDKN1A, SCARB2, and RPS27A. This network provides significant insights into their functional roles and their potential as therapeutic targets. Additionally, an examination of immune infiltration demonstrated significant differences in the quantities of resting natural killer (NK) cells and M2 macrophages between SARC samples and control samples. CDKN1A displayed a positive correlation with M2 macrophages and an inverse relationship with resting NK cells. The results show how important the immune microenvironment is to the spread of SARC, suggesting promising pathways for the creation of immunotherapeutic strategies. Our research elucidates the molecular pathways implicated in SARC and establishes a foundation for future therapeutic approaches. However, additional validation is crucial to translating these findings into viable clinical applications.