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Review
. 2024 Sep 20:17:6563-6581.
doi: 10.2147/JIR.S489682. eCollection 2024.

Deciphering the Role of LncRNAs in Osteoarthritis: Inflammatory Pathways Unveiled

Kangyi Hu  1 , Haonan Wen  1 , Ting Song  1 , Zhixin Che  1 , Yongjia Song  1 , Min Song  1
Affiliations
Review

Deciphering the Role of LncRNAs in Osteoarthritis: Inflammatory Pathways Unveiled

Kangyi Hu et al. J Inflamm Res. .

Abstract

Long non-coding RNA (LncRNA), with transcripts over 200 nucleotides in length, play critical roles in numerous biological functions and have emerged as significant players in the pathogenesis of osteoarthritis (OA), an inflammatory condition traditionally viewed as a degenerative joint disease. This review comprehensively examines the influence of LncRNA on the inflammatory processes driving OA progression, focusing on their role in regulating gene expression, cellular activities, and inflammatory pathways. Notably, LncRNAs such as MALAT1, H19, and HOTAIR are upregulated in OA and exacerbate the inflammatory milieu by modulating key signaling pathways like NF-κB, TGF-β/SMAD, and Wnt/β-catenin. Conversely, LncRNA like MEG3 and GAS5, which are downregulated in OA, show potential in dampening inflammatory responses and protecting against cartilage degradation by influencing miRNA interactions and cytokine production. By enhancing our understanding of LncRNA' roles in OA inflammation, we can better leverage them as potential biomarkers for the disease and develop innovative therapeutic strategies for OA management. This paper aims to delineate the mechanisms by which LncRNA influence inflammatory responses in OA and propose them as novel targets for therapeutic intervention.

Keywords: LncRNA; chondrocytes; inflammation; osteoarthritis; pro-inflammatory factors.

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Conflict of interest statement

The authors have no relevant financial or non-financial interests to disclose.

Figures

Figure 1
Figure 1
The mechanism of inflammation in OA: In osteoarthritis (OA), inflammatory factors such as IL-1β, IL-6, and TNF-α trigger inflammation by activating multiple signaling pathways, including the TLR/NF-κB, p38 MAPK, JAK/STAT3, and Wnt pathways. The TLR/NF-κB pathway promotes inflammation through the activation of IKK, while the p38 MAPK pathway exacerbates inflammation via JNK and Wnt signaling, and the JAK/STAT3 pathway is influenced by TNF-α and ROS. These inflammatory signals work together to cause pathological changes such as cartilage degradation, synovial hyperplasia, subchondral osteosclerosis, and osteophyte formation, thus accelerating the progression of OA. Created with BioRender.com.
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Grants and funding

The work was supported by Gansu University of Chinese Medicine to introduce a talent research start-up fund (2024YJRC-09) and The 2024 Gansu Basic Research Program-Natural Science Funds-Youth Science and Technology Fund (24JRRA567).

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