ArticleClinical interventions in aging2026
Causal Implication of CD52-Driven Immune Dysregulation in Sarcopenic Obesity: Integrating Mendelian Randomization and Multiomics Profiling.
Article in Clinical interventions in aging, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- Inhibition of TWEAK/Fn14 Ameliorates Sarcopenic Obesity by Restoring Mitochondrial Biogenesis via the AMPK/SIRT1/PGC-1α Axis.Diabetes, metabolic syndrome and obesity : targets and therapy · 2026Article
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Authors and funding
8 authors.
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Abstract
Purpose: Sarcopenic obesity patients are likely to develop exacerbated metabolic dysfunction, while the mechanism linking sarcopenia and obesity is still unclear. This study aims to explore hub genes and immune-metabolic dysregulation related to the molecular pathogenesis of sarcopenia and obesity. Methods: We used a public Gene Expression Omnibus (GEO) dataset to identify hub genes associated with sarcopenia and obesity. Weighted gene co-expression network analysis (WGCNA), protein-protein interaction (PPI), differentially expressed gene (DEG) analysis, GO/KEGG functional enrichment analyses and immune cell infiltration analysis were conducted to identify hub genes. Subsequently, these hub genes underwent multi-level validation. Results: Integrated bioinformatics analysis identified 16 shared hub genes linked to the sarcopenia-obesity nexus. These genes were mainly enriched in immune-related pathways, as supported by immune infiltration profiling. External validation in independent cohorts confirmed CD52 as a common and central gene in both sarcopenia and obesity datasets, showing significant associations with immune cell characteristics. Mendelian randomization analysis indicated potential causal links between genetically predicted CD52 levels and reduced hand grip strength as well as increased body mass index, and these results were further supported by PCR assays in clinical samples. Conclusion: The integrative analysis indicates that CD52 may function as a novel immunometabolic mediator in SO pathogenesis, underscoring its potential as a candidate biomarker for further study.
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