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JNK pathway in osteoarthritis: pathological and therapeutic aspects
Hong-Xing Ge1, Fu-Man Zou1, Yan Li2
1a Department of Orthopaedics , Second People's Hospital of Jingmen , Jingmen , China.
Context:
Osteoarthritis (OA) is a common chronic degenerative joint disease resulting in physical disability and reduced quality of life. Different biochemical signaling pathways are involved in the progression of OA, including the c-Jun NH2-terminal kinase (JNK) signal transduction pathway.
Objective:
In this study, we have reviewed the recent updates on the association of JNK pathway with OA.
Methods:
In this review, we have explored the databases like PubMed, Google Scholar, Medline, Scopus, etc., and collected the most relevant papers of JNK signaling pathway involved in the pathogenesis and therapeutics of OA Results: JNK has been shown by scientific studies to be activated (phosphorylated) in OA that can play a key role in the cartilage destruction. Activation of JNK causes the phosphorylation of c-Jun that causes decreased proteoglycan synthesis and enhanced production of matrix metalloproteinase 13 (MMP-13). Overproduction of MMP-13 by chondrocytes plays a central role in cartilage degeneration in OA. Thus, targeting JNK pathway might be a promising therapeutic application for the prevention and treatment of OA. A number of JNK-inhibitors have been used in vitro and in vivo studies; however, not yet been translated into human use.
Conclusions:
This review study indicates that JNK pathway plays an important role in development and progression of OA, and targeting the JNK pathway might be a potential approach for the treatment of OA in future.
Insights
The c-Jun NH2-terminal kinase (JNK) pathway is activated in osteoarthritis (OA), contributing to cartilage destruction. Targeting this JNK pathway shows promise for future OA treatment.
Area of Science:
- Biochemistry
- Molecular Biology
- Rheumatology
Background:
- Osteoarthritis (OA) is a prevalent degenerative joint disease impacting physical function and quality of life.
- The c-Jun NH2-terminal kinase (JNK) signal transduction pathway is implicated in OA progression.
Purpose of the Study:
- To review recent findings on the association between the JNK pathway and osteoarthritis.
- To explore the role of JNK signaling in OA pathogenesis and potential therapeutic strategies.
Main Methods:
- Comprehensive literature search of databases including PubMed, Google Scholar, Medline, and Scopus.
- Identification and collection of relevant studies on JNK signaling in OA.
Main Results:
- JNK activation (phosphorylation) is observed in OA and plays a critical role in cartilage degradation.
- Activated JNK leads to c-Jun phosphorylation, reducing proteoglycan synthesis and increasing matrix metalloproteinase 13 (MMP-13) production.
- Overproduction of MMP-13 by chondrocytes is a key factor in OA cartilage degeneration.
Conclusions:
- The JNK pathway is significantly involved in the development and progression of OA.
- Targeting the JNK pathway represents a potential future therapeutic strategy for OA treatment.
- While JNK inhibitors have shown promise in preclinical studies, human translation is pending.
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