ArticleActa pharmacologica Sinica2022
CDDO-Im ameliorates osteoarthritis and inhibits chondrocyte apoptosis in mice via enhancing Nrf2-dependent autophagy.
Article in Acta pharmacologica Sinica, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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17 citing papers in PubMed, 32 citations in OpenAlex.
- HDAC3 represses Nrf2-GDF11 signaling to drive chondrocyte adipogenesis in temporomandibular joint osteoarthritis.Journal of advanced research · 2026Article
- Identification of a putative progenitor-like chondrocyte subpopulation in osteoarthritic human cartilage.Stem cell research & therapy · 2026Article
- The Nrf2/HO-1 signaling pathway in arthritis: from molecular mechanisms to therapeutic potential.Frontiers in cell and developmental biology · 2026Review
- Revealing the Diagnostic Potential of Three RHO GTPase-Related Genes in Osteoarthritis Based on Single-Cell RNA Sequencing and GEO Dataset Analysis.International journal of genomics · 2026Article
- Review
- Intermittent fasting in osteoarthritis: from mechanistic insights to therapeutic potential.Frontiers in nutrition · 2025Review
- NRF2 in age-related musculoskeletal diseases: Role and treatment prospects.Genes & diseases · 2024Review
- Anti-Inflammatory and Antioxidant Effects of Irigenen Alleviate Osteoarthritis Progression through Nrf2/HO-1 Pathway.Pharmaceuticals (Basel, Switzerland) · 2024Article
- Luteolin regulating synthesis and catabolism of osteoarthritis chondrocytes via activating autophagy.Heliyon · 2024Article
- Melatonin Delays Arthritis Inflammation and Reduces Cartilage Matrix Degradation through the SIRT1-Mediated NF-κB/Nrf2/TGF-β/BMPs Pathway.International journal of molecular sciences · 2024Article
- MicroRNA-204-5p Ameliorates Renal Injury via Regulating Keap1/Nrf2 Pathway in Diabetic Kidney Disease.Diabetes, metabolic syndrome and obesity : targets and therapy · 2024Article
- Disease-modifying interactions between chronic kidney disease and osteoarthritis: a new comorbid mouse model.RMD open · 2023Article
- Isoginkgetin-loaded reactive oxygen species scavenging nanoparticles ameliorate intervertebral disc degeneration via enhancing autophagy in nucleus pulposus cells.Journal of nanobiotechnology · 2023Article
- Autophagy in the pathogenesis and therapeutic potential of post-traumatic osteoarthritis.Burns & trauma · 2023Review
- Mitochondrial proteotoxicity: implications and ubiquitin-dependent quality control mechanisms.Cellular and molecular life sciences : CMLS · 2022Review
- The role of autophagy and ferroptosis in sensorineural hearing loss.Frontiers in neuroscience · 2022Review
- Oroxin B alleviates osteoarthritis through anti-inflammation and inhibition of PI3K/AKT/mTOR signaling pathway and enhancement of autophagy.Frontiers in endocrinology · 2022Article
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11 authors at 3 institutions in 1 country.
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Abstract
Osteoarthritis (OA) is the most prevalent chronic degenerative joint disease with few treatment options. The pathogenesis of OA is characterized by sustained inflammation, oxidative stress and chondrocyte apoptosis that eventually lead to cartilage degradation and joint dysfunction. In the present study, we identified a synthetic triterpenoid CDDO-Im(1-[2-cyano-3,12-dioxooleana-1,9(11)-dien-28-oyl] imidazole) as an activator of Nrf2 (nuclear factor erythroid 2-related factor 2) that displayed strong anti-OA effects. We showed that CDDO-Im (20 nM) significantly alleviated TNF-α-induced apoptosis of primary human chondrocytes and extracellular matrix degradation. In a mouse OA model incurred by DMM (destabilization of medial meniscus), administration of CDDO-Im (2.5 mg/kg, ip, every other day for 8 weeks) effectively reduced knee joint cartilage erosion and serum levels of inflammatory cytokines IL-1β and IL-6. We revealed that CDDO-Im (20 nM) significantly enhanced autophagy activities in chondrocytes, whereas the autophagy inhibition by chloroquine (CQ, 50 μM) or 3-methyladenine (3-MA, 5 mM) abrogated the anti-apoptosis and chondroprotective effects of CDDO-Im in TNF-α-treated chondrocytes. Moreover, we confirmed that CDDO-Im (1-20 nM) dose-dependently activated Nrf2 pathway in TNF-α-treated chondrocytes, and its chondroprotective and autophagy-enhancing effects were significantly diminished when Nrf2 signaling was blocked by Nrf2 inhibitor ML385 (20 μM) or siRNA-mediated Nrf2 knockdown. Together, our results demonstrate that CDDO-Im exhibits prominent chondroprotective and anti-OA activities owing to its Nrf2 activation and autophagy-enhancing properties, which might provide new insights into the strategies of OA clinical prevention and treatment.
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