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Characterizing programmed cell death features in osteoarthritis through integrative multiomics and machine learning

Qinchao Sun1, Ye Zhong1, Gaoxiang Huang1

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|October 15, 2025
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Summary

Programmed cell death (PCD) genes are altered in osteoarthritis (OA), with S100A9, PMAIP1, and EDA2R as risk factors and FASN as protective. PCD shows diagnostic potential and therapeutic implications for OA.

Keywords:
ImmunoinfiltrationMachine learningOsteoarthritisProgrammed cell death

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Area of Science:

  • Biochemistry
  • Genetics
  • Immunology

Background:

  • Programmed cell death (PCD) is vital for tissue homeostasis but its role in osteoarthritis (OA) is unclear.
  • Signaling molecules impact metabolism and disease, yet their specific involvement in OA pathogenesis requires elucidation.

Purpose of the Study:

  • To systematically evaluate the predictive value, genetic alterations, and therapeutic implications of PCD-associated genes in OA.
  • To investigate the diagnostic efficacy and immune infiltration related to PCD genes in OA.

Main Methods:

  • Multiomics analyses including transcriptomic and single-cell transcriptome data were performed.
  • Weighted gene co-expression network analysis and machine learning models were employed to identify key PCD genes.
  • An in vitro OA model using hypoxic ATDC5 chondrocytes was utilized to study gene expression and function.

Main Results:

  • S100A9, PMAIP1, and EDA2R were upregulated in OA, suggesting them as risk factors, while FASN was downregulated, indicating a protective role.
  • PCD demonstrated reliable diagnostic accuracy for OA.
  • Downregulation of S100A9, PMAIP1, EDA2R and overexpression of FASN ameliorated hypoxia-induced cellular damage and inflammation in vitro.

Conclusions:

  • PCD genes have significant roles in OA pathogenesis and progression.
  • AI-driven analysis of PCD genes offers potential for individualized OA vulnerability assessments and therapeutic strategies.
  • Abnormal expression of four hub PCD genes provides new research avenues for OA and immune-mediated diseases.