Integrative multi-omics identifies MSR1 as a programmed cell death and extracellular matrix hub gene in osteoarthritis with hesperidin targeting potential - Scorecard - MDSpire

Integrative multi-omics identifies MSR1 as a programmed cell death and extracellular matrix hub gene in osteoarthritis with hesperidin targeting potential

  • By

  • Bao, Jinquan

  • Wu, Lingling

  • Zhao, Wenqiang

  • Li, Bo

  • Li, Zilong

  • Bai, Zhigang

  • Ma, Penglei

  • Gao, Bo

  • Qiao, Chenggang

  • March 30, 2026

  • 0 min

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Clinical Scorecard: Multi-Omics Analysis Reveals MSR1 as a Central Gene in Programmed Cell Death and Extracellular Matrix Dynamics in Osteoarthritis with Potential for Hesperidin Targeting

At a Glance

CategoryDetail
ConditionOsteoarthritis (OA)
Key MechanismsProgrammed cell death (PCD) and extracellular matrix (ECM) dynamics
Target PopulationPatients with Osteoarthritis
Care SettingClinical and research settings

Key Highlights

  • MSR1 identified as a key gene in OA pathogenesis through multi-omics analysis.
  • 517 genes associated with OA enriched in immune and developmental pathways.
  • MSR1 expression higher in OA samples than in healthy samples with AUC > 0.7.
  • Hesperidin identified as a high-affinity MSR1-binding compound.
  • MSR1 promotes apoptosis and ECM degradation in OA-like chondrocytes.

Guideline-Based Recommendations

Diagnosis

  • Utilize RNA-seq data and weighted gene co-expression network analysis for OA diagnosis.

Management

  • Consider hesperidin as a potential therapeutic agent targeting MSR1 in OA.

Monitoring & Follow-up

  • Monitor MSR1 expression levels in OA patients to assess disease progression.

Risks

  • Increased MSR1 expression may correlate with enhanced apoptosis and ECM degradation.

Patient & Prescribing Data

Individuals diagnosed with Osteoarthritis

Hesperidin may provide a novel therapeutic approach by targeting MSR1.

Clinical Best Practices

  • Incorporate multi-omics approaches in OA research for better understanding of disease mechanisms.
  • Evaluate the role of immune modulation in OA treatment strategies.

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