ArticleCell death & disease2022
CircFOXO3 protects against osteoarthritis by targeting its parental gene FOXO3 and activating PI3K/AKT-mediated autophagy.
Article in Cell death & disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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Who cites it
49 citing papers in PubMed, 69 citations in OpenAlex.
- Effects of probiotics on joint homeostasis and osteoarthritis: Development of microbe-gut-cartilage axis-on-a-chip.Science advances · 2026Article
- OIP5-AS1 Sponges miR-223-3p to Upregulate FoxO3 and Ameliorate Temporomandibular Joint Osteoarthritis by Inhibiting Chondrocyte Apoptosis.Journal of cellular and molecular medicine · 2026Article
- Circular RNAs orchestrate molecular networks in osteoarthritis: From miRNA sponging to epigenetic and exosome-mediated regulation.Molecular biology reports · 2026Review
- Network Pharmacology and Experimental Validation Reveal Wu Miao Pill's Therapeutic Effects on Acute Gouty Arthritis Through P2X7R Regulation.Biochemical genetics · 2026Article
- Melatonin Exerts Chondroprotective Effects Against Osteoarthritis by Promoting PI3K/AKT/FoxO3-Mediated Mitophagy.The Kaohsiung journal of medical sciences · 2026Article
- Review
- CircFN1 modulates IL-1β-induced osteoarthritis through the miR-19b-3p/PTEN signaling axis.Scientific reports · 2026Article
- Circ-FoxO3 alleviates APOE4-induced brain pathology through FoxO3-mediated autophagy.Molecular genetics and genomics : MGG · 2026Article
- Programmed cell death in osteoarthritis.Apoptosis : an international journal on programmed cell death · 2026Review
- Effects of TGMXD-208, a Novel PI3K Inhibitor, on Adjuvant-induced Arthritis Rats by Suppressing PI3K/AKT Signaling PathwayEndocrine, metabolic & immune disorders drug targets · 2026Article
- Isoviolanthin suppresses IL-1β-induced inflammatory and catabolic responses in chondrocytes.Frontiers in pharmacology · 2026Article
- The dual role of autophagy in cartilage degradation: from mechanisms to targeted therapeutics.Frontiers in cell and developmental biology · 2026Review
- LncRNA-Histone Modification Crosstalk: Orchestrating Cancer Pathobiology.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Comparison of the therapeutic efficacy of leukocyte-poor and leukocyte-rich platelet-rich plasma in rabbit knee osteoarthritis and the study of autophagy mechanism.BMC musculoskeletal disorders · 2025Article
- Epigenetic Regulation of Aging and its Rejuvenation.MedComm · 2025Review
- Forkhead box O proteins in chondrocyte aging and diseases.Journal of orthopaedic translation · 2025Review
- EIF4A3-induced circPRKAR1B promotes esophageal squamous cell carcinoma progression through binding PKM2 to regulate NF-κB induced CCL3 secretion.Cancer cell international · 2025Article
- Research progress of circular RNA FOXO3 in diseases (review).Global medical genetics · 2025Review
- CircTBCK protects against osteoarthritis by regulating extracellular matrix and autophagy.Human cell · 2025Article
- CircSPG21 ameliorates oxidative stress-induced senescence in nucleus pulposus-derived mesenchymal stem cells and mitigates intervertebral disc degeneration through the miR-217/SIRT1 axis and mitophagy.Stem cell research & therapy · 2025Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Osteoarthritis (OA) is a degenerative joint disorder causing pain and functional disability. Emerging evidence reveals that circular RNAs (circRNAs) play essential roles in OA progression and development. This study aimed to investigate the role of a novel circRNA factor, circFOXO3, in the progression of OA and elucidate its underlying molecular mechanism. The function of circFOXO3 in OA and interaction between circFOXO3 and its downstream mRNA target, forkhead box O3 (FOXO3), were evaluated by western blot (WB), immunofluorescence (IF), RNA immunoprecipitation, reverse transcription-quantitative PCR (RT-qPCR), and fluorescence in situ hybridization (FISH). Upregulation of circFOXO3 and autophagic flux were detected both in vivo and in vitro by WB, transmission electron microscopy (TEM), IF, and immunohistochemistry (IHC). A mouse model of OA was also used to confirm the role of circFOXO3 in OA pathogenesis in vivo. Decreased expression of circFOXO3 in OA cartilage tissues was directly associated with excessive apoptosis and imbalance between anabolic and catabolic factors of the extracellular matrix (ECM). Mechanistically, circFOXO3 functioned in cartilage by targeting its parental gene FOXO3 and activating autophagy. Intra-articular injection of lentivirus-circFOXO3 alleviated OA in the mouse model. In conclusion, our results reveal the key role played by circFOXO3 in OA progression; circFOXO3 overexpression may alleviate apoptosis of chondrocytes and promote anabolism of the ECM via activation of FOXO3 and autophagy, providing a potentially effective novel therapeutic strategy for OA.
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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.