The single-cell transcription reveals the aberrant differentiation trajectory of chondrocytes in the intervertebral disc for congenital scoliosis.

Junfeng Wang, Haodong Li, Dong Fu, Yiming Zheng, Chuang Qian, Lin Li, Maoxiang Qian, Dahui Wang

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Article in iScience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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8 authors.

Junfeng WangDepartment of Orthopedics, Children's Hospital of Fudan University, Shanghai 201102, P.R. China.

Haodong LiDepartment of Orthopedics, Children's Hospital of Fudan University, Shanghai 201102, P.R. China.

Dong FuDepartment of Orthopedics, Children's Hospital of Fudan University, Shanghai 201102, P.R. China.

Yiming ZhengDepartment of Orthopedics, Children's Hospital of Fudan University, Shanghai 201102, P.R. China.

Chuang QianDepartment of Orthopedics, Children's Hospital of Fudan University, Shanghai 201102, P.R. China.

Lin LiDepartment of Hematology and Oncology, Children's Hospital of Fudan University, and Shanghai Key Laboratory of Medical Epigenetics, Institutes of Biomedical Sciences, Fudan University, Shanghai 201102, P.R. China.

Maoxiang QianDepartment of Hematology and Oncology, Children's Hospital of Fudan University, and Shanghai Key Laboratory of Medical Epigenetics, Institutes of Biomedical Sciences, Fudan University, Shanghai 201102, P.R. China.

Dahui WangDepartment of Orthopedics, Children's Hospital of Fudan University, Shanghai 201102, P.R. China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cartilage endplate (CEP) in the intervertebral disc (IVD) contributes to vertebral level asymmetrically in congenital scoliosis (CS). However, the cellular compositions of CEP and the subsequent alteration of cellular environment in its neighboring annulus fibrosus and nucleus pulposus remain unknown during the progressive scoliosis. Herein, this study resolved the single-cell landscape of IVD in CS. Chondrocytes in CS demonstrated a different trajectory and were enriched in the cytoskeleton dependent cytokinesis pathways. H19, ECRG4, CCN1, and CCN2 were the specific markers for CS, and DBP may be the critical transcription factor (TF) for CS. Notochord and pericyte were the dominative cell types in the cell-cell communications, among which NCAM and SEMA5 signaling were the unique pathways for CS. Collectively, the aberrant differentiation trajectory of chondrocytes may explain the vertebral dysplasia in CS, and these critical gene markers, TFs, and pathways identified in this study may provide potential therapeutic targets for CS.

Indexed as

pathophysiologytranscriptomics

Identifiers

PMID40502710

DOI10.1016/j.isci.2025.112608

PMCPMC12152652

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