ArticleFrontiers in immunology2025
Single-cell RNA-seq reveals a repair pattern in cystic lesions in steroid induced osteonecrosis of the femoral head.
Article in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Macrophage immunometabolic reprogramming in inflammatory repair failure in osteonecrosis of the femoral head.Journal of orthopaedic translation · 2026Review
- Single-cell RNA sequencing analysis revealed a potential association between ELK3 expression and the progression of multiple myeloma.Frontiers in immunology · 2026Article
- Unraveling Non-coding RNAs and dysregulation of TGF-β signalling in cardiorenal syndrome, a focused review for molecular and clinical applications.Molecular biology reports · 2025Review
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Authors and funding
13 authors.
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Abstract
Background: Studies have indicated that cystic lesions play a crucial role in the repair processes of steroid-induced osteonecrosis of the femoral head and its subsequent collapse. Here, we employed single-cell RNA sequencing (scRNA-seq) technology to investigate the transcriptomic landscape and repair mechanisms of cystic lesions in SIONFH. Methods: We applied scRNA-seq combined with computational approaches to characterize distinct cell subsets and their molecular signatures within cystic lesions from three SIONFH patients. Additionally, histological assays were conducted to observe pathological manifestations of these lesions. Results: Eight cell types were identified in cystic lesions of SIONFH. Among them, chondrocytes were divided into five subgroups. Among them, chondrocytes were divided into five subgroups: homeostatic chondrocytes (HomC), fibrocartilage chondrocytes (FC), prehypertrophic chondrocytes (preHTC), inflammatory chondrocytes (InflamC), and hypertrophic chondrocytes (HTC). Additionally, histological assays showed the presence of chondrocytes and a transition zone from chondrocytes to bone tissue within the cystic lesions. Notably, we report that one of the HTC clusters with CLIC3+ expression exhibited a strong involved in bone mineralization, osteoblast differentiation, and cell differentiation. Conclusion: We have delineated the cellular heterogeneity and molecular signatures of cystic lesions in SIONFH. The results reveal a distinct repair program within these lesions, which might be driven by chondrocyte hypertrophy and might culminate in osteogenic differentiation.
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