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Integrative multi-omics identifies MSR1 as a programmed cell death and extracellular matrix hub gene in

Jinquan Bao1, Lingling Wu2, Wenqiang Zhao1

  • 1The Second Affiliated Hospital of Inner Mongolia Medical University, Hohhot, Inner Mongolia Autonomous, China.

Frontiers in Immunology
|June 8, 2026
PubMed
Abstract

Insights

Osteoarthritis involves programmed cell death and extracellular matrix changes. This study identifies MSR1 as a key gene in OA pathogenesis, suggesting hesperidin as a potential treatment.

Area of Science:

  • Molecular Biology
  • Genetics
  • Immunology

Background:

  • Osteoarthritis (OA) is a degenerative joint disease with complex molecular underpinnings.
  • Programmed cell death (PCD) and extracellular matrix (ECM) remodeling are implicated in OA pathogenesis.
  • Identifying key genes in OA is crucial for understanding disease mechanisms.

Purpose of the Study:

  • To identify a key programmed cell death/extracellular matrix-related gene in osteoarthritis (OA) pathogenesis.
  • To investigate the role of the identified gene in OA progression.
  • To explore potential therapeutic agents for OA.

Main Methods:

  • Multi-omics analysis including RNA-seq and weighted gene co-expression network analysis (WGCNA).
  • Differential expression analysis, protein-protein interaction (PPI) network construction, and regulatory network prediction.
  • In vitro studies using an IL-1β-induced OA cell model and molecular docking for drug discovery.

Main Results:

  • MSR1 was identified as a key OA-associated PCD/ECM-related gene.
  • MSR1 expression is elevated in OA tissues and correlates with immune cell populations.
  • In vitro, MSR1 promotes chondrocyte apoptosis, ECM degradation, and NF-κB pathway activation; hesperidin shows high-affinity binding to MSR1.

Conclusions:

  • MSR1 is a central regulator in osteoarthritis pathogenesis, involving programmed cell death and extracellular matrix.
  • MSR1's role in immune modulation offers insights into OA mechanisms.
  • Hesperidin is proposed as a potential therapeutic agent for OA targeting MSR1.
Keywords:
MSR1WGCNAextracellular matrixhesperidinimmune microenvironmentmolecular dockingosteoarthritisprogrammed cell death

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