ArticleAging cell2021
JUNB-FBXO21-ERK axis promotes cartilage degeneration in osteoarthritis by inhibiting autophagy.
Article in Aging cell, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
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Who cites it
56 citing papers in PubMed, 97 citations in OpenAlex.
- Targeting E3 Ubiquitin Ligases in Post-Traumatic Osteoarthritis: Therapeutic Opportunities and Pharmacological Perspectives.Pharmaceutics · 2026Review
- CircGRHL2 suppresses EMT and enhances sunitinib sensitivity in ccRCC via the miR-330-5p/FBXO21 axis.Cellular and molecular life sciences : CMLS · 2026Article
- CILP Inhibits hyaline cartilage fibrosis and chondrocyte ferroptosis via keap1-Nrf2 axis in early osteoarthritis exercise therapy.Cellular and molecular life sciences : CMLS · 2026Article
- Programmed cell death in osteoarthritis.Apoptosis : an international journal on programmed cell death · 2026Review
- Research hotspots and prospects on the correlation between subchondral bone and stem cells: bibliometrics and visual analysis.Frontiers in surgery · 2026Review
- Article
- Single-cell RNA sequencing of cerebrospinal fluid immune cells in relapsing-remitting multiple sclerosis: insights into cellular composition and immune dynamics.Journal of neurology · 2025Article
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- PPARγ controls ESCRT-dependent fibroblast-like synoviocyte exosome biogenesis and alleviates chondrocyte osteoarthritis mediated by exosomal ANXA1.Journal of orthopaedic translation · 2025Article
- RO5126766 attenuates osteoarthritis by inhibiting osteoclastogenesis and protecting chondrocytes through mediating the ERK pathway.Journal of orthopaedic translation · 2025Article
- sdRNA-D43 derived from small nucleolar RNA snoRD43 improves chondrocyte senescence and osteoarthritis progression by negatively regulating PINK1/Parkin-mediated mitophagy pathway via dual-targeting NRF1 and WIPI2.Cell communication and signaling : CCS · 2025Article
- [Lupeol Alleviates Chondrocytes Senescence in Osteoarthritis by Regulating Autophagy via the Sirtuin 3/Mechanistic Target of Rapamycin Kinase Pathway].Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2025Article
- Review
- Characterization of gene expression profiles in Alzheimer's disease and osteoarthritis: A bioinformatics study.PloS one · 2025Article
- Exploring the biological functions and immune regulatory roles of IRAK3, TNFRSF1A, CX3CR1, and JUNB in T2DM combined with MAFLD: integrated bioinformatics and single-cell analysis.Frontiers in immunology · 2025Article
- The multifaceted roles of E3 ubiquitin ligases in osteoarthritis.Frontiers in cell and developmental biology · 2025Review
- Article
- Modulating Autophagy in Osteoarthritis: Exploring Emerging Therapeutic Drug Targets.International journal of molecular sciences · 2024Review
- Identifying critical modules and biomarkers of intervertebral disc degeneration by using weighted gene co-expression network.JOR spine · 2024Article
- Ubiquitination and deubiquitination: Implications for the pathogenesis and treatment of osteoarthritis.Journal of orthopaedic translation · 2024Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Osteoarthritis (OA) is a heterogeneous disease that is extremely hard to cure owing to its complex regulation network of pathogenesis, especially cartilage degeneration. FBXO21 is a subunit of ubiquitin E3 ligases that degrades P-glycoprotein and EID1 by ubiquitination and activates the JNK and p38 pathways; however, its role in OA remains unknown. Here, the main objective of this study was to evaluate the potential effects and mechanism of FBXO21 in OA degeneration, we revealed that FBXO21 is upregulated in the cartilage of patients with OA, aging, and monosodium iodoacetate-induced OA rats, and chondrocytes treated with interleukin-1β, tumor necrosis factor-α, and lipopolysaccharide. Moreover, the in vivo and in vitro knockdown of FBXO21 suppressed OA-related cartilage degeneration, as evidenced by activated autophagy, upregulated anabolism, alleviated apoptosis, and downregulated catabolism. In contrast, its overexpression promoted OA-related cartilage degeneration. In addition, using mass spectrometry and co-immunoprecipitation assay, we demonstrated that the downstream mechanism of FBXO21 inhibits autophagy by interacting with and phosphorylating ERK. Furthermore, FBXO21 alleviated anabolism and enhanced apoptosis and catabolism by inhibiting autophagy in rat chondrocytes. Interestingly, for its upstream mechanism, JUNB promoted FBXO21 expression by directly targeting the FBXO21 promoter, thus further accelerating cartilage degeneration in SW1353 cells and rat chondrocytes. Overall, our findings reveal that the JUNB-FBXO21-ERK axis regulates OA apoptosis and cartilage matrix metabolism by inhibiting autophagy. Therefore, FBXO21 is an attractive target for regulating OA pathogenesis, and its knockdown may provide a novel targeted therapy 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.