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已发表论文
焦亡在骨关节炎发病机制中的作用：最新综述
Authors Yang F , Li D, Long W, Li E, Wei B
Received 16 June 2025
Accepted for publication 3 October 2025
Published 29 October 2025 Volume 2025:18 Pages 15065—15079
DOI https://doi.org/10.2147/JIR.S547458
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 2
Editor who approved publication: Dr Ujjwol Risal
Fengrui Yang,* Debin Li,* Wei Long, Ermao Li, Bo Wei
Institute of Translational Medicine, School of Basic Medical, Hengyang Medical College, University of South China, Hengyang Central Hospital, Hengyang, Hunan, 421001, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Bo Wei, Institute of Translational Medicine, School of Basic Medical, Hengyang Medical College, University of South China, Hengyang Central Hospital, Hengyang, Hunan, 421001, People’s Republic of China, Tel +8618640130803, Email usc-wb@usc.edu.cn
Abstract: Osteoarthritis (OA), a prevalent degenerative inflammatory joint disorder, imposes a substantial global health burden, affecting over 500 million people worldwide and representing a leading cause of pain and disability. Its pathogenesis is characterized by the progressive degradation of articular cartilage, concomitant synovitis, and aberrant subchondral bone remodeling. Contemporary management strategies primarily aim to alleviate symptoms rather than halt disease progression, underscoring the critical need to elucidate fundamental pathogenic mechanisms to identify novel therapeutic targets. Recently, pyroptosis—a lytic, pro-inflammatory cell death mediated by inflammasomes (eg, NLRP3) and gasdermin D (GSDMD)— has emerged as a key mechanism linking inflammation to tissue damage. This review integrates pyroptosis research with OA pathomechanisms to establish their interplay. This review synthesizes contemporary research to delineate the intricate interplay between pyroptosis and OA pathomechanisms across joint tissues. Our integration of evidence reveals that: (1) The pyroptosis-inflammation axis involves NLRP3 activation, caspase cleavage, and GSDMD pore formation, releasing IL-1β/IL-18 that amplify synovitis and tissue destruction; (2) Chondrocyte pyroptosis is regulated by NF-κB and Hedgehog signaling, suppressible by inhibitors (eg, loganin); (3) Synovial cells undergo pyroptosis under stimuli like LPS, perpetuating fibrosis via HIF-1α activation; (4) Subchondral bone pyroptosis disrupts remodeling, targetable via PI3K/AKT pathways.
Keywords: osteoarthritis, pyroptosis, pathomechanism, Mechanism
Institute of Translational Medicine, School of Basic Medical, Hengyang Medical College, University of South China, Hengyang Central Hospital, Hengyang, Hunan, 421001, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Bo Wei, Institute of Translational Medicine, School of Basic Medical, Hengyang Medical College, University of South China, Hengyang Central Hospital, Hengyang, Hunan, 421001, People’s Republic of China, Tel +8618640130803, Email usc-wb@usc.edu.cn
Abstract: Osteoarthritis (OA), a prevalent degenerative inflammatory joint disorder, imposes a substantial global health burden, affecting over 500 million people worldwide and representing a leading cause of pain and disability. Its pathogenesis is characterized by the progressive degradation of articular cartilage, concomitant synovitis, and aberrant subchondral bone remodeling. Contemporary management strategies primarily aim to alleviate symptoms rather than halt disease progression, underscoring the critical need to elucidate fundamental pathogenic mechanisms to identify novel therapeutic targets. Recently, pyroptosis—a lytic, pro-inflammatory cell death mediated by inflammasomes (eg, NLRP3) and gasdermin D (GSDMD)— has emerged as a key mechanism linking inflammation to tissue damage. This review integrates pyroptosis research with OA pathomechanisms to establish their interplay. This review synthesizes contemporary research to delineate the intricate interplay between pyroptosis and OA pathomechanisms across joint tissues. Our integration of evidence reveals that: (1) The pyroptosis-inflammation axis involves NLRP3 activation, caspase cleavage, and GSDMD pore formation, releasing IL-1β/IL-18 that amplify synovitis and tissue destruction; (2) Chondrocyte pyroptosis is regulated by NF-κB and Hedgehog signaling, suppressible by inhibitors (eg, loganin); (3) Synovial cells undergo pyroptosis under stimuli like LPS, perpetuating fibrosis via HIF-1α activation; (4) Subchondral bone pyroptosis disrupts remodeling, targetable via PI3K/AKT pathways.
Keywords: osteoarthritis, pyroptosis, pathomechanism, Mechanism