CHI3L1 regulates chondrocytes function via JAK2/STAT3 signaling pathway during lumbar facet joint degeneration

Purpose : Low back pain (LBP) is a global public health concern closely linked to lumbar facet joint (FJ) degeneration, yet its specific pathogenesis remains unclear. CHI3L1 (chitinase 3 like 1) is involved in inflammation and tissue remodeling, but its role in FJ degeneration is poorly understood. This study aimed to investigate the correlation between CHI3L1 and lumbar FJ degeneration, clarify its regulatory effects on chondrocyte functions, and explore the underlying molecular mechanisms. Methods : Forty human lumbar FJ cartilage tissues were collected to detect CHI3L1 expression via RT-qPCR. In vitro experiments were performed on human chondrocytes treated with recombinant CHI3L1 protein or CHI3L1 siRNA, including cell proliferation, cell cycle, apoptosis, ELISA and western blot. Protein expression microarray was used to identify downstream signaling pathways. In vivo experiments were conducted on FJ degeneration rat models injected with sh-CHI3L1 vector, followed by HE staining for histopathological observation. Results : We found CHI3L1 expression was significantly elevated in degenerated FJ cartilage and positively correlated with degeneration stages. In vitro, CHI3L1 inhibited chondrocyte proliferation, induced G1 phase arrest, promoted apoptosis, and upregulated the expression of inflammatory cytokines (IL-1β, IL-6, IL-8, TNF-α). Silencing CHI3L1 reversed these effects. Mechanistically, CHI3L1 regulated inflammatory cytokine expression through activating the JAK2/STAT3 signaling pathway. In vivo, knockdown of CHI3L1 significantly attenuated FJ degeneration in rats. Conclusions : CHI3L1 plays a pivotal role in lumbar FJ degeneration by regulating chondrocyte viability and inflammatory responses via the JAK2/STAT3 signaling pathway. CHI3L1 may serve as a potential biomarker and therapeutic target for FJ degenerative diseases.