ArticleInternational journal of surgery (London, England)2026
Potential regulators and metabolic networks of muscle fatty infiltration: genomic and radiomics investigation based on 33 300 participants.
Article in International journal of surgery (London, England), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Integrative Analysis Uncover the Effects and Multi-Omics Features of Thigh Muscle Fat Infiltration.Aging cell · 2026Article
- Association Between Catenin Beta-1 (CTNNB1) Gene Polymorphisms and Non-Traumatic Osteonecrosis of the Femoral Head (ONFH).Current issues in molecular biology · 2026Article
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Authors and funding
9 authors.
Funding
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Abstract
backgroundMuscle fatty infiltration (MFI), the pathological replacement of muscle by adipose tissue in chronic diseases, lacks comprehensive genetic characterization despite known cellular contributors. Elucidating its genetic architecture and clinical correlations could reveal therapeutic targets for this debilitating condition. MATERIALS AND
methodsWe performed a genome-wide association study (GWAS) on 33 300 participants' genomic/MRI data, identifying MFI-associated loci. Fine-mapping (GCTA-COJO/FUMA), Mendelian randomization (tissue-specific genes, plasma proteins, metabolites) and genetic correlation (LDSC) analyses were conducted. KLF5's functional role was validated through inhibition experiments in fibro-adipogenic progenitors (FAPs) and murine immobilization-induced MFI models.
resultsGWAS revealed 91 significant SNPs across 26 loci, with risk genes enriched in olfactory transduction and JAK-STAT pathways. Multi-omics integration identified KLF5 as a key transcriptional regulator, CHRDL2/HLA-E as circulating risk protein, and phosphatidylcholines/triglycerides as causal metabolites, and genetic correlations between MFI and metabolic/musculoskeletal disorders. Experimentally, KLF5 suppression reduced adipo-fibrogenic FAP differentiation and improved muscle histology in mice.
conclusionOur study delineates MFI's polygenic basis, establishes clinical-metabolic relationships, and mechanistically validates KLF5 as a target. These findings provide a framework for treating MFI through metabolic modulation or KLF5 inhibition, with broader implications for muscle-degenerative comorbidities.
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