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Effect of AGEs on human disc herniation: intervertebral disc hernia is also effected by AGEs
Michiyo Tsuru1, Kensei Nagata, Atsuo Jimi
1Department of Orthopaedic Surgery, Kurume University School of Medicine, Kurume 830-0011, Japan. michiyo@med.kurume-u.ac.jp
Abstract:
Currently, extracellular matrix MMP has been discussed in relation to the extrusion and spontaneous regression of the herniated mass observed in lumbar disc herniation. However, the question remains as to whether degenerated protein is really the cause of this condition's pathogenesis. We confirmed immunologically by means of electron microscopy that extrusion is caused by the AGEs (advanced glycation end products)-induced cross-linking of collagen, and that spontaneous regression is due to AGE receptors on macrophages. Further, AGEs were found to be already exposed during histogenesis, suggesting a relation to apoptosis. In lumbar disc herniation and aging, glucose-derived AGEs cross-link proteins and cause vascular tissue damage.
Insights
Advanced glycation end products (AGEs) cause collagen cross-linking, leading to herniated disc extrusion. Macrophage AGE receptors drive spontaneous regression, linking AGEs to disc degeneration and aging.
Area of Science:
- Biochemistry
- Cell Biology
- Orthopedics
Background:
- Extracellular matrix metalloproteinases (MMPs) are implicated in lumbar disc herniation (LDH) pathogenesis.
- The precise role of protein degeneration in LDH remains unclear.
Purpose of the Study:
- To investigate the role of advanced glycation end products (AGEs) in LDH.
- To elucidate the mechanisms behind herniated disc extrusion and spontaneous regression.
Main Methods:
- Immunological confirmation using electron microscopy.
- Analysis of AGEs and AGE receptors on macrophages.
Main Results:
- Extrusion in LDH is caused by AGEs-induced collagen cross-linking.
- Spontaneous regression is mediated by AGE receptors on macrophages.
- AGEs are present during histogenesis, suggesting a link to apoptosis.
Conclusions:
- Glucose-derived AGEs contribute to protein cross-linking and vascular damage in LDH and aging.
- AGEs play a critical role in the pathogenesis of lumbar disc herniation.