ArticleRedox biology2020
Advanced oxidation protein products increase TNF-α and IL-1β expression in chondrocytes via NADPH oxidase 4 and accelerate cartilage degeneration in osteoarthritis progression.
Article in Redox biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers, 1 of them a synthesis that pooled it.
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Who cites it
75 citing papers in PubMed, 1 synthesis or guideline pooled it, 146 citations in OpenAlex.
- Efficacy and immune-inflammatory mechanism of acupuncture-related therapy in animal models of knee osteoarthritis: a preclinical systematic review and network meta-analysis.Journal of orthopaedic surgery and research · 2024Pooled it
- Signal-driven interplay between lipid peroxidation and ferroptosis orchestrates osteoarthritis degeneration.Journal of orthopaedic translation · 2026Review
- Osteoarthritis: Epidemiology, Diagnosis, and Treatment.MedComm · 2026Review
- Lnc-CHRM4-2:1 Inhibits M2 Polarization and Efferocytosis of Macrophages by Downregulating MerTK and SLC2A1 in Rheumatoid Arthritis.Journal of immunology research · 2026Article
- Correlation of radiographic and histopathological changes with IL-17 and advanced oxidation protein products in knee osteoarthritic individuals with metabolic syndrome.Innovative surgical sciences · 2025Article
- Synovial mesenchymal stem cell-derived exosomes delivering GRPEL1 activate PINK1-mediated mitophagy to promote cartilage repair in arthritis.World journal of stem cells · 2025Article
- Antioxidant functionalized double-net/TA dynamic hydrogel promotes cartilage regeneration through stabilization of chondrocyte phenotype.Materials today. Bio · 2025Article
- Postoperative Changes in Hematological, Biochemical, and Redox Status Parameters in Spinal Osteoarthritis Patients Undergoing Spinal Decompression and Stabilization Surgery.Journal of clinical medicine · 2025Article
- Forkhead box O proteins in chondrocyte aging and diseases.Journal of orthopaedic translation · 2025Review
- Radiological-behavioral disparities in experimental osteoarthritis: Sex-specific progression and therapeutic response in a rat model.Veterinary world · 2025Article
- Anti-osteoarthritis effect of a standardizedNutrition research and practice · 2025Article
- Inhibition of WAC alleviates the chondrocyte proinflammatory secretory phenotype and cartilage degradationActa pharmaceutica Sinica. B · 2025Article
- Unleashing the potential of exercise: conquering cardiovascular disease by targeting inflammasome activation.European journal of medical research · 2025Review
- The interplay between driver mutation and oxidative stress in colorectal cancer: from pathogenesis to therapeutics.Journal of translational medicine · 2025Review
- Integrated network pharmacology reveals the mechanism of action of Xianlinggubao prescription for inflammation in osteoarthritis.BMC complementary medicine and therapies · 2025Article
- SOX4 accelerates intervertebral disc degeneration via EZH2/NRF2 pathway in response to mitochondrial ROS-dependent NLRP3 inflammasome activation in nucleus pulposus cells.Journal of translational medicine · 2025Article
- Accumulation of advanced oxidation protein products aggravates bone-fat imbalance during skeletal aging.Journal of orthopaedic translation · 2025Article
- Mechanism of action and new developments in the study of curcumin in the treatment of osteoarthritis: a narrative review.Inflammopharmacology · 2025Review
- CombiningFrontiers in cell and developmental biology · 2025Article
- Protective Effects of Vitamin D on Proteoglycans of Human Articular Chondrocytes through TGF-β1 Signaling.Nutrients · 2024Article
15 more citing papers are in PubMed but not listed here.
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Interleukin (IL)-1β and tumor necrosis factor (TNF)-α, in particular, control the degeneration of articular cartilage, making them prime targets for osteoarthritis (OA) therapeutic strategies. Advanced oxidation protein products (AOPPs) are prevalent in numerous diseases. Our previous work demonstrates that intra-articular injections of AOPPs accelerate regression of cartilage in OA models. Whether AOPPs exist in the course of OA and their effects on TNF-α and IL-1β expression in chondrocytes are still unclear. This study confirmed that AOPPs levels in human synovial fluid were positively associated with severity of OA. We also found AOPPs deposition in articular cartilage in anterior cruciate ligament transection (ACLT) induced rodent OA models. AOPPs increased expression of TNF-α and IL-1β in chondrocytes in vitro, which was inhibited by pre-treatment with SB202190 (p38-MAPK inhibitor) or apocynin (NADPH oxidase inhibitor) or NOX4 knockdown by siRNAs. Subsequently, we further verified in vivo that exogenous injection of AOPPs in OA mice up-regulated expression of TNF-α and IL-1β in cartilage, which was blocked by treatment with apocynin. In parallel, apocynin attenuated articular cartilage degeneration resulting in substantially lower OARSI scores. Specifically, apocynin reduced NOX4, p-P38, TNF-α and IL-1β and increased collagen II and glycosaminoglycan (GAG). This study demonstrated that AOPPs increased expression of TNF-α and IL-1β in chondrocytes via the NADPH oxidase4-dependent and p38-MAPK mediated pathway, and accelerated cartilage degeneration in OA progression. These findings suggest an endogenous pathogenic role of AOPPs in OA progression. Targeting AOPPs-triggered cellular mechanisms might be a promising therapeutic option for patients with 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.