ArticleBMC musculoskeletal disorders2025
Knockdown of CLEC4D alleviates myoblast dysfunction and inflammation in sarcopenia by inhibiting the JAK/STAT pathway.
Article in BMC musculoskeletal disorders, 2025. 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.
- Decoding vascular calcification-neutrophil signature in pathogenesis of chronic IgA nephropathy: evidence from artificial intelligence-driven multi-omics andFrontiers in physiology · 2026Article
- Sarcopenia independently predicts acute cholecystitis in older patients with gallstones: a retrospective cohort study.Frontiers in medicine · 2026Article
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5 authors.
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Abstract
objectiveSarcopenia is a progressive skeletal muscle disease that is prevalent among the elderly. We aim to explore the role of the C-type lectin domain containing 4, member D (CLEC4D) in sarcopenia.
methodsHub genes were identified from protein-protein interaction networks based on differentially expressed genes from GSE145480 and GSE139204 datasets. Sarcopenia in mice was induced by Dexamethasone. Pathological estimation was conducted using hematoxylin-eosin and Masson staining. Myoblasts were treated with D-galactose (D-gal) to induce senescence, which was assessed by senescence-associated β-galactosidase staining. The viability and apoptosis were evaluated using the Cell Counting Kit-8 assay and flow cytometry. Protein and gene expression were examined by western blot and real-time quantitative polymerase chain reaction. Enzyme-linked immunosorbent assays were performed to measure inflammatory factors.
resultsWe identified 8 hub genes associated with sarcopenia, among which CCL5, CLEC4D, LGALS3, ESR2, FCGR4, and CLEC4N were upregulated in sarcopenia. CLEC4D knockdown enhanced myogenic differentiation, suppressed muscular fibrosis and atrophy, and alleviated sarcopenia in mice via reducing inflammatory cytokine levels. CLEC4D knockdown attenuated D-gal-induced myoblast dysfunction by enhancing differentiation and downregulating the expression of inflammatory cytokines and muscle atrophy markers. The Janus kinase/signal transducer and activator of transcription (JAK/STAT) pathway was activated in D-gal-induced myoblasts. CLEC4D knockdown inhibited the JAK/STAT pathway in D-gal-induced myoblasts. Notably, an activator of the JAK/STAT pathway reversed the inhibitory effect of CLEC4D knockdown on D-gal-induced myoblast dysfunction and inflammation.
conclusionTargeting CLEC4D represents a promising therapeutic strategy for sarcopenia, as its knockdown suppresses disease progression by inhibiting the JAK/STAT signaling pathway.
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