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Saturated Fatty Acids Induce Ceramide-associated Macrophage Cell Death
Published on: October 31, 2017
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Ceramide accumulation accelerates nucleus pulposus cells degradation by p38MAPK activation
1Department of Orthopedics, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China.
European Review for Medical and Pharmacological Sciences
|September 6, 2021
Summary
This study on nucleus pulposus cell degradation has been withdrawn due to data inaccuracies. Further research is needed to understand ceramide accumulation and p38 mitogen-activated protein kinase (MAPK) activation in intervertebral disc degeneration.
Area of Science:
- Biochemistry
- Cell Biology
- Orthopedics
Background:
- Intervertebral disc degeneration is a complex process.
- Cellular senescence and apoptosis contribute to disc degradation.
- Lipid metabolism, including ceramide accumulation, may play a role.
Purpose of the Study:
- To investigate the role of ceramide accumulation in nucleus pulposus cell degradation.
- To explore the involvement of p38 mitogen-activated protein kinase (MAPK) signaling pathway.
Main Methods:
- Cell culture models of nucleus pulposus cells.
- Measurement of ceramide levels.
- Assessment of cell viability and apoptosis.
- Western blot analysis for p38MAPK pathway activation.
Main Results:
- Ceramide accumulation was observed in degrading nucleus pulposus cells.
- Increased p38MAPK activation correlated with ceramide accumulation.
- Inhibition of p38MAPK showed a protective effect on cells.
Conclusions:
- Ceramide accumulation appears to accelerate nucleus pulposus cell degradation.
- The p38MAPK pathway is implicated in this process.
- Targeting ceramide metabolism or p38MAPK may offer therapeutic potential.
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