Regulation and therapy, the role of JAK2/STAT3 signaling pathway in OA: a systematic review
Bo Chen1, Ke Ning1, Ming-Li Sun1
1College of Exercise and Health, Shenyang Sport University, Shenyang, China.
Abstract:
Osteoarthritis (OA) is a multifactorial chronic disease primarily characterized by the degeneration of articular cartilage. Currently, there is a lack of effective treatments for OA other than surgery. The exploration of the mechanisms of occurrence is important in exploring other new and effective treatments for OA. The current evidence shows that the Janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) signaling pathway plays a vital role in cytogenesis and is involved in OA progression. The terms "JAK2", "STAT3", and "Osteoarthritis"were used in a comprehensive literature search in PubMed to further investigate the relationship between the JAK2/STAT3 signaling pathway and OA. This review focuses on the role and mechanism of JAK2/STAT3 signaling in cartilage degradation, subchondral bone dysfunction, and synovial inflammation. In addition, this review summarizes recent evidence of therapeutic approaches to treat OA by targeting the JAK2/STAT3 pathway to accelerate the translation of evidence into the progression of strategies for OA treatment. Video abstract.
Insights
The Janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) pathway is crucial in osteoarthritis (OA) progression. Targeting this pathway offers promising new therapeutic strategies for OA treatment beyond surgery.
Area of Science:
- Biomedical Science
- Molecular Biology
- Pathology
Background:
- Osteoarthritis (OA) is a degenerative joint disease with limited non-surgical treatment options.
- Understanding OA pathogenesis is critical for developing novel therapeutic interventions.
- The Janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) pathway is implicated in cellular processes relevant to OA.
Approach:
- A comprehensive literature search was conducted using "JAK2", "STAT3", and "Osteoarthritis" in PubMed.
- This review synthesizes current evidence on the JAK2/STAT3 pathway's role in OA.
- Focus is placed on mechanisms in cartilage degradation, subchondral bone, and synovitis.
Key Points:
- The JAK2/STAT3 pathway significantly contributes to articular cartilage degeneration in OA.
- Dysregulation of JAK2/STAT3 signaling impacts subchondral bone integrity and function.
- Synovial inflammation in OA is influenced by the JAK2/STAT3 signaling cascade.
Conclusions:
- The JAK2/STAT3 pathway is a key mediator in the multifaceted progression of osteoarthritis.
- Targeting the JAK2/STAT3 pathway presents a viable strategy for developing new OA treatments.
- Further research into JAK2/STAT3 inhibitors could accelerate clinical translation for OA therapy.
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