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A Proinflammatory, Degenerative Organ Culture Model to Simulate Early-Stage Intervertebral Disc Disease.
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Galectin-4: A Novel Mediator of Human Intervertebral Disc Degeneration

Christine Strauss1,2, Daniel Djojic1, Johannes Stadlmann3

  • 1Karl Chiari Lab for Orthopaedic Biology, Department of Orthopedics and Trauma Surgery Medical University of Vienna Vienna Austria.

JOR Spine
|August 7, 2026
PubMed
Abstract

Insights

Galectin-4 is linked to intervertebral disc degeneration, activating pathways that promote disease. This finding highlights galectin-4 as a key factor in disc degeneration pathogenesis.

Area of Science:

  • Biochemistry
  • Cell Biology
  • Musculoskeletal Research

Background:

  • Intervertebral disc (IVD) degeneration causes chronic back pain.
  • Galectins, carbohydrate-binding proteins, can promote disease markers in musculoskeletal tissues.
  • The role of galectin-4 and -8 in IVD degeneration was previously uninvestigated.

Purpose of the Study:

  • To investigate the presence and function of galectin-4 and -8 in human intervertebral disc degeneration.
  • To correlate galectin expression with degeneration severity.
  • To explore the in vitro effects of galectins on IVD cells.

Main Methods:

  • Immunohistochemistry of 36 human IVD specimens.
  • Correlation of galectin scores with radiological (Pfirrmann) and histopathological (Rutges) degeneration.
  • In vitro studies using annulus fibrosus (AF) and nucleus pulposus (NP) cell cultures treated with recombinant galectins or IL-1β.
  • Analysis via RT-qPCR, In-Cell Western, and mass spectrometry for galectin binding sites.

Main Results:

  • Galectin-4 presence correlated with IVD degeneration severity; galectin-8 did not.
  • Both galectins activated the NF-κB pathway and induced disease markers (CXCL8, MMP3) in vitro.
  • Nucleus pulposus cells showed higher sensitivity to galectins and IL-1β compared to annulus fibrosus cells.

Conclusions:

  • Galectin-4 is identified as a novel molecular player in intervertebral disc degeneration pathogenesis.
  • Galectin-4's role in promoting disease markers suggests it as a potential therapeutic target.

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