ArticleGlobal spine journal2023
Mechanism of the Mitogen-Activated Protein Kinases/Mammalian Target of Rapamycin Pathway in the Process of Cartilage Endplate Stem Cell Degeneration Induced by Tension Load.
Article in Global spine journal, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 11 citations in OpenAlex.
- Targeting skeletal interoception: a novel mechanistic insight into intervertebral disc degeneration and pain management.Journal of orthopaedic surgery and research · 2025Review
- Lipid metabolic disorders and their impact on cartilage endplate and nucleus pulposus function in intervertebral disk degeneration.Frontiers in nutrition · 2025Review
- Stress-Activated Protein Kinases in Intervertebral Disc Degeneration: Unraveling the Impact of JNK and p38 MAPK.Biomolecules · 2024Review
- The JNK signaling pathway in intervertebral disc degeneration.Frontiers in cell and developmental biology · 2024Review
- Review
- Intervertebral Disc Progenitors: Lessons Learned from Single-Cell RNA Sequencing and the Role in Intervertebral Disc Regeneration.Bioengineering (Basel, Switzerland) · 2023Article
- Cartilage Endplate-Derived Stem Cells for Regeneration of Intervertebral Disc Degeneration: An Analytic Study.Journal of inflammation research · 2023Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
STUDY
designBasic Research.
objectiveIntervertebral disc degeneration (IVDD) is caused by the cartilage endplate (CEP). Cartilage endplate stem cell (CESC) is involved in the recovery of CEP degeneration. Tension load (TL) contributes a lot to the initiation and progression of IVDD. This study aims to investigate the regulatory mechanism of the Mitogen-activated protein kinases/Mammalian target of rapamycin (MAPK/mTOR) pathway during TL-induced CESC degeneration.
methodsCESCs were isolated from New Zealand big-eared white female rabbits (6 months old). FX-4000T cell stress loading system was applied to establish a TL-induced degeneration model of CESCs. Western blotting was used to detect the level of mTOR pathway-related proteins and autophagy markers LC3-Ⅱ, Beclin-1, and p62 in degenerative CESCs. The expression of MAPK pathway-related proteins JNK and extracellular signal-regulated kinases (ERK) in degenerated CESCs was inhibited by cell transfection to explore whether JNK and ERK play a regulatory role in TL-induced autophagy in CESCs.
resultsIn the CESC degeneration model, the mTOR pathway was activated. After inhibition of mTOR, the autophagy level of CESCs was increased, and the degeneration of CESCs was alleviated. The MAPK pathway was also activated in the CESC degeneration model. Inhibition of JNK expression may alleviate TL-induced CEP degeneration by inhibiting Raptor phosphorylation and activating autophagy. Inhibition of ERK expression may alleviate TL-induced CEP degeneration by inhibiting mTOR phosphorylation and activating autophagy.
conclusionInhibition of JNK and ERK in the MAPK signaling family alleviated TL-induced CESC degeneration by inhibiting the phosphorylation of Raptor and mTOR in the mTOR pathway.
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