Effects of selenium-mediated RUNX2 overexpression and its transcriptome alterations on Chondrocyte injury in Kashin Beck disease.

Di Zhang, Qiang Li, Xiaoli Yang, Yongmin Xiong, Shiquan Sun

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Article in Frontiers in cell and developmental biology, 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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5 · Who and what money

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5 authors.

Di ZhangNational and Local Joint Engineering Research Center of Biodiagnosis and Biotherapy, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, China.

Qiang LiInstitute of Endemic Diseases and Key Laboratory of Trace Elements and Endemic Diseases, School of Public Health, Xi'an Jiaotong University Health Science Center, Xi'an, Shaanxi, China.

Xiaoli YangShaanxi Provincial Key Laboratory of Infection and Immune Diseases, Shaanxi Provincial People's Hospital, Xi'an, Shaanxi, China.

Yongmin XiongInstitute of Endemic Diseases and Key Laboratory of Trace Elements and Endemic Diseases, School of Public Health, Xi'an Jiaotong University Health Science Center, Xi'an, Shaanxi, China.

Shiquan SunInstitute of Endemic Diseases and Key Laboratory of Trace Elements and Endemic Diseases, School of Public Health, Xi'an Jiaotong University Health Science Center, Xi'an, Shaanxi, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Objective: Kashin-Beck disease (KBD) is a nutrition-related osteoarthropathy characterized by excessive apoptosis and matrix destruction. Micronutrient selenium (Se) deficiency is recognized as a major environmental risk factor. This study aimed to investigate the role of RUNX2 in cartilage injury associated with KBD. Methods: RUNX2 expression in articular cartilage from KBD patients was assessed by immunohistochemistry. Results: The proportion of RUNX2-positive cells in KBD cartilage was significantly higher than in controls. Conclusion: Micronutrient Se deficiency may contribute to the pathogenesis of KBD by modulating RUNX2 expression and inducing excessive chondrocyte apoptosis, while Se supplementation exerts a protective effect. RUNX2 plays a critical role in KBD progression and may represent a potential therapeutic target.

Indexed as

Chondrocyte injuryKashin-Beck diseaseRNA transcription profilesRUNX2selenium deficiency

Identifiers

PMID41425094

DOI10.3389/fcell.2025.1687954

PMCPMC12714888

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