ArticleScientific reports2025
Integrated transcriptomic analysis identifies lysosomal autophagy-related genes in sarcopenia.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
2 citing papers in PubMed.
- Co-morbid biomarkers for sarcopenic obesity associated with gut microbiota metabolites: From burden to treatment.PLoS computational biology · 2026Article
- From homeostasis to pathology, organelle-specific autophagy in skeletal muscle: a PRISMA-ScR scoping review.Frontiers in physiology · 2026Review
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Authors and funding
4 authors.
Funding
Abstract
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.
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