ArticleInternational journal of molecular medicine2019
MicroRNA‑93 inhibits chondrocyte apoptosis and inflammation in osteoarthritis by targeting the TLR4/NF‑κB signaling pathway.
Article in International journal of molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 91 papers.
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Who cites it
91 citing papers in PubMed, 138 citations in OpenAlex.
- Efficacy and potential toxicity of Duhuo Qinjiao Decoction in osteoarthritis via the NF-κB pathway.Clinical rheumatology · 2026Article
- Epigenetic regulation in osteoarthritis: recent updates and emerging mechanisms.Frontiers in genetics · 2026Review
- 1,25(OH)Clinical rheumatology · 2025Article
- Programmed Cell Death of Chondrocytes, Synovial Cells, Osteoclasts, and Subchondral Bone Cells in Osteoarthritis.Journal of inflammation research · 2025Review
- Therapeutic prospects and potential mechanisms of Prdx6: as a novel target in musculoskeletal disorders.Frontiers in physiology · 2025Review
- Non-coding RNA in cartilage regeneration: regulatory mechanism and therapeutic strategies.Frontiers in bioengineering and biotechnology · 2025Review
- Review
- Dexamethasone relieves the inflammatory response caused by inguinal hernia meshes through miR-155.Hernia : the journal of hernias and abdominal wall surgery · 2024Article
- Liraglutide, a glucagon-like peptide-1 receptor agonist, ameliorates inflammation and apoptosis via inhibition of receptor for advanced glycation end products signaling in AGEs induced chondrocytes.BMC musculoskeletal disorders · 2024Article
- Exosome miR-4738-3p-mediated regulation ofBiomolecules & biomedicine · 2024Article
- microRNA-105-5p protects against chondrocyte injury, extracellular matrix degradation, and osteoarthritis progression by targeting SPARCL1.Histology and histopathology · 2024Article
- [miR-515-5p targeting Toll-like receptor 4 regulates myeloid differentiation primary response gene 88/nuclear factor-kappa B pathway to inhibit apoptosis and inflammatory response of osteoarthritis chondrocytes].Zhongguo xiu fu chong jian wai ke za zhi = Zhongguo xiufu chongjian waike zazhi = Chinese journal of reparative and reconstructive surgery · 2024Article
- Saikosaponin D alleviates inflammatory response of osteoarthritis and mediates autophagy via elevating microRNA-199-3p to target transcription Factor-4.Journal of orthopaedic surgery and research · 2024Article
- MicroRNA-93-5p regulates odontogenic differentiation and dentin formation via KDM6B.Journal of translational medicine · 2024Article
- Unraveling the path to osteoarthritis management: targeting chondrocyte apoptosis for therapeutic intervention.Frontiers in cell and developmental biology · 2024Review
- Evidence supported by Mendelian randomization: impact on inflammatory factors in knee osteoarthritis.Frontiers in medicine · 2024Article
- Macrophage polarization in spinal cord injury repair and the possible role of microRNAs: A review.Heliyon · 2023Review
- Mir-25-3p in extracellular vesicles from fibroblast-like synoviocytes alleviates pyroptosis of chondrocytes in knee osteoarthritis.Journal of bioenergetics and biomembranes · 2023Article
- GREM1, LRPPRC and SLC39A4 as potential biomarkers of intervertebral disc degeneration: a bioinformatics analysis based on multiple microarray and single-cell sequencing data.BMC musculoskeletal disorders · 2023Article
- Article
31 more citing papers are in PubMed but not listed here.
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5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Osteoarthritis (OA) is a serious disease of the articular cartilage, and inflammation has been implicated in its pathogenesis. Previously, microRNAs (miRNAs) have been proposed as novel regulators of inflammation, however, the functional role of microRNAs in regulating inflammation in OA remains to be fully elucidated. The aim of the present study was to investigate the roles of miRNAs in OA inflammation and the underlying molecular mechanism. Firstly, the miRNA expression patterns were analyzed in the articular cartilage tissues from experimental OA mice using an miRNA microarray. miRNA (miR)‑93 was identified with particular interest due to its reported effects on apoptosis and inflammation suppression. Subsequently, the expression of miR‑93 was further validated in the articular cartilage tissues of OA mice and lipopolysaccharide (LPS)‑stimulated primary chondrocytes. Using this LPS‑induced chondrocyte injury model, the overexpression of miR‑93 enhanced cell viability, improved cell apoptosis and attenuated the inflammatory response, as reflected by reductions in pro‑inflammatory cytokines, including tumor necrosis factor (TNF)‑α, interleukin (IL)‑1β and IL‑6. In addition, Toll‑like receptor 4 (TLR4), an important regulator of the nuclear factor‑κB (NF‑κB) signaling pathway, was identified as a direct target of miR‑93 in chondrocytes. Furthermore, the restoration of TLR4 markedly abrogated the inhibitory effects of miR‑93 on the chondrocyte apoptosis and inflammation induced by LPS. In addition, the overexpression of miR‑93 by agomir‑miR‑93 significantly inhibited the levels of pro‑inflammatory cytokines and cell apoptosis, whereas antagomir‑93 exacerbated apoptosis and inflammation in vivo. Taken together, the results of the study suggested that miR‑93 may be a promising therapeutic target for the treatment of human OA.
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