Regulation and therapy, the role of JAK2/STAT3 signaling pathway in OA: a systematic review

被引:49
|
作者
Chen, Bo [1 ]
Ning, Ke [1 ]
Sun, Ming-li [1 ]
Zhang, Xin-an [1 ]
机构
[1] Shenyang Sport Univ, Coll Exercise & Hlth, Shenyang, Peoples R China
关键词
Osteoarthritis; JAK2/STAT3; Pathway; Mechanism; Targeted therapy; NF-KAPPA-B; CALCIUM-PHOSPHATE CRYSTALS; RAT CHONDROCYTES; LEPTIN RECEPTOR; IN-VITRO; OSTEOARTHRITIS; CARTILAGE; EXPRESSION; APOPTOSIS; MECHANISMS;
D O I
10.1186/s12964-023-01094-4
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
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.
引用
收藏
页数:14
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