ArticleArthritis research & therapy2023
FTO-mediated m6A demethylation of pri-miR-3591 alleviates osteoarthritis progression.
Article in Arthritis research & therapy, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 27 citations in OpenAlex.
- IGF2BP3 Overexpression Accelerates Osteoarthritis Progression by Promoting Glycolysis via mThe Kaohsiung journal of medical sciences · 2026Article
- FTO in Bone Diseases: Functions, Mechanisms and Therapeutic Potential.Biomolecules · 2026Review
- Deficiency of the mCellular and molecular life sciences : CMLS · 2026Article
- Association of single nucleotide polymorphisms in FILIP1-SENP6 and FTO with temporomandibular joint osteoarthritis: clinical and in silico study.Scientific reports · 2026Article
- Downregulation of FTO aggravates osteoarthritis with obesity by erasing mMilitary Medical Research · 2026Article
- Inhibition of the METTL3/mThe journal of headache and pain · 2025Article
- Joint Tissues: Convergence and Divergence of the Pathogenetic Mechanisms of Rheumatoid Arthritis and Osteoarthritis.International journal of molecular sciences · 2025Review
- FTOZhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2025Article
- RNA Modifications in Osteoarthritis: Epitranscriptomic Insights into Pathogenesis and Therapeutic Targets.International journal of molecular sciences · 2025Review
- From bone marrow mesenchymal stem cells to diseases: the crucial role of mStem cell research & therapy · 2025Review
- M6A Modified miR-31-5p Suppresses M1 Macrophage Polarization and Autoimmune Dry Eye by Targeting P2RX7.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Therapeutic Potential of FTO Demethylase in Metabolism and Disease Pathways.The protein journal · 2025Review
- Mechanistic and therapeutic insights into the function of N6-methyladenosine in arthritic diseases.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Review
- Novel Insights into the Regulatory Role of N6-Methyladenosine in the Pathogenesis and Clinical Treatment of Osteoarthritis: Research Status and Prospect.Journal of inflammation research · 2025Review
- Spatiotemperal Dynamics of Osteoarthritis: Bridging Insights from Bench to Bedside.Aging and disease · 2024Review
- Procyanidin capsules provide a new option for long-term ROS scavenging in chronic inflammatory diseases.Materials today. Bio · 2024Article
- Obesity-induced downregulation of miR-192 exacerbates lipopolysaccharide-induced acute lung injury by promoting macrophage activation.Cellular & molecular biology letters · 2024Article
- Recent advances of m6A methylation in skeletal system disease.Journal of translational medicine · 2024Review
- Regulation of ferroptosis in osteoarthritis and osteoarthritic chondrocytes by typical MicroRNAs in chondrocytes.Frontiers in medicine · 2024Review
- The Role of Genetics and Epigenetic Regulation in the Pathogenesis of Osteoarthritis.International journal of molecular sciences · 2023Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesIncreasing evidence have demonstrated the N6-methyladenosine (m MATERIALS AND
methodsThe FTO expression was detected in mice OA cartilage tissues and lipopolysaccharide (LPS)-stimulated chondrocytes. Gain-of-function assays was used to evaluate the role of FTO in OA cartilage injury in vitro and in vivo. The miRNA-sequencing, RNA-binding protein immunoprecipitation (RIP), luciferase reporter assay, and in vitro pri-miRNA processing assays were conducted to confirm that FTO modulated the pri-miR-3591 process in an m6A-dependent manner and then the binding sites of miR-3591-5p with PRKAA2.
resultsFTO was outstandingly downregulated in LPS-stimulated chondrocytes and OA cartilage tissues. FTO overexpression enhanced the proliferation, suppressed apoptosis, and decreased degradation of extracellular matrix in LPS-induced chondrocytes, whereas FTO knockdown contributed to the opposite effects. In vivo animal experiments showed that FTO overexpression markedly alleviated OA mice cartilage injury. Mechanically, FTO-mediated m6A demethylation of pri-miR-3591 leaded to a maturation block of miR-3591-5p, which relieved the inhibitory effect of miR-3591-5p on PRKAA2 and then promoted the increase of PRKAA2, thereby alleviating OA cartilage damage.
conclusionsOur results attested that FTO alleviated the OA cartilage damage by mediating FTO/miR-3591-5p/PRKAA2 axis, which provided fresh insights into the therapeutic strategies for OA.
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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.