ArticleBioscience reports2019
LncRNA SNHG1 alleviates IL-1β-induced osteoarthritis by inhibiting miR-16-5p-mediated p38 MAPK and NF-κB signaling pathways.
Article in Bioscience reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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Who cites it
45 citing papers in PubMed, 66 citations in OpenAlex.
- Review
- Beyond miRNA Cargo Profiles: Anti-Inflammatory Roles of Extracellular Vesicle-Enriched miRNAs Derived From Human Intervertebral Disc Cells Unveiled by Functional Testing.Journal of extracellular biology · 2026Article
- Article
- Non-viral gene delivery systems for osteoarthritis therapy.Biomaterials translational · 2026Review
- Protective Effects of miR-16-5p and miR-142-3p on Inflammation and Autophagy in Human Corneal Epithelial Cells Under Hyperosmotic Stress In Vitro.International journal of molecular sciences · 2025Article
- MAPK Pathway Activation Patterns in the Synovium Reveal ERK1/2 and EGFR as Key Players in Osteoarthritis.Biomedicines · 2025Article
- Revealing the regulatory role of lncRNAs SNHG1 and CRNDE on Th17/Treg imbalance in diabetic kidney disease.Clinical and experimental medicine · 2025Article
- Oxidative Stress, MicroRNAs, and Long Non-Coding RNAs in Osteoarthritis Pathogenesis: Cross-Talk and Molecular Mechanisms Involved.International journal of molecular sciences · 2025Review
- CRNDE alleviates IL-1β-induced chondrocyte damage by modulating miR-31/NF-κB pathway.Journal of orthopaedic surgery and research · 2024Article
- Circulating microRNA Profiles Identify a Patient Subgroup with High Inflammation and Severe Symptoms in Schizophrenia Experiencing Acute Psychosis.International journal of molecular sciences · 2024Article
- LncRNA-mediated cartilage homeostasis in osteoarthritis: a narrative review.Frontiers in medicine · 2024Review
- LncRNA SNHG1 knockdown inhibits hyperglycemia induced ferroptosis via miR-16-5p/ACSL4 axis to alleviate diabetic nephropathy.Journal of diabetes investigation · 2023Article
- Bioinformatics analysis of synovial fluid-derived mesenchymal stem cells in the temporomandibular joint stimulated with IL-1β.Cytotechnology · 2023Article
- Advances in Research on the Regulatory Roles of lncRNAs in Osteoarthritic Cartilage.Biomolecules · 2023Review
- The emerging role of lncRNAs in osteoarthritis development and potential therapy.Frontiers in genetics · 2023Review
- Matrix metalloproteinases in rheumatoid arthritis and osteoarthritis: a state of the art review.Reumatologia · 2023Review
- Key Genes Associated with Pyroptosis in Gout and Construction of a miRNA-mRNA Regulatory Network.Cells · 2022Article
- Engineering of MSC-Derived Exosomes: A Promising Cell-Free Therapy for Osteoarthritis.Membranes · 2022Review
- Exosomal long noncoding RNAs - the lead thespian behind the regulation, cause and cure of autophagy-related diseases.Molecular biology reports · 2022Review
- SNHG1-miR-186-5p-YY1 feedback loop alleviates hepatic ischemia/reperfusion injury.Cell cycle (Georgetown, Tex.) · 2022Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Long non-coding RNA (LncRNA) small nucleolar RNA host gene 1 (SNHG1) has been reported in the occurrence and development of several diseases, but its biological role and mechanism in osteoarthritis (OA) remain to be illuminated. In the present research, we aimed to investigate the effect of SNHG1 on IL-1β-induced OA and its molecular mechanism. Results revealed that SNHG1 decreased the expression of MMPs, ADAMTs, collagen, and aggrecan, and ameliorates IL-1β-induced metabolic dysfunction in normal human chondrocytes-keen. In addition, SNHG1 inhibited the expressions of pro-inflammatory cytokines in chondrocytes, including NO, PGE2, IL-6, TNF-α, i-NOS, and COX-2. Furthermore, luciferase reporter assay demonstrated that SNHG1 could directly interact with miR-16-5p and suppressed miR-16-5p expression and activity. What is more, miR-16-5p overexpression reversed SNHG1-inhibited aberrant catabolism and inflammation triggered by IL-1β stimulation. Finally, SNHG1 inhibits the expression of miR-16-5p-mediated factors involved in p38MAPK and NF-κB signaling pathways, including ERK1/2, p-p38 and p-p65. Taken together, the results of our studies illuminate that SNHG1 alleviates the inflammation of IL-1β-induced OA through the activation of miR-16-5p-mediated p38MAPK and NF-κB signaling pathway. It suggested that SNHG1 may serve as a potential target for OA diagnosis and treatment.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.