ArticlePloS one2013
Advanced glycation end products induce peroxisome proliferator-activated receptor γ down-regulation-related inflammatory signals in human chondrocytes via Toll-like receptor-4 and receptor for advanced glycation end products.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 47 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
47 citing papers in PubMed, 104 citations in OpenAlex.
- Serum pentosidine concentration is associated with radiographic severity of lumbar spondylosis in a general Japanese population.Journal of bone and mineral metabolism · 2017Trial
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- Mechanisms of AGE-induced VSMC phenotypic switching and macrophage modulation in human abdominal aortic aneurysms.Experimental biology and medicine (Maywood, N.J.) · 2025Article
- Identification and validation of up-regulated TNFAIP6 in osteoarthritis with type 2 diabetes mellitus.Scientific reports · 2024Article
- Advanced glycation end products promote meniscal calcification by activating the mTOR-ATF4 positive feedback loop.Experimental & molecular medicine · 2024Article
- Article
- Cabozantinib prevents AGEs-induced degradation of type 2 collagen and aggrecan in human chondrocytes.Aging · 2023Article
- Advanced Glycation End Products and Activation of Toll-like Receptor-2 and -4 Induced Changes in Aquaporin-3 Expression in Mouse Keratinocytes.International journal of molecular sciences · 2023Article
- Pioglitazone-Loaded Cartilage-Targeted Nanomicelles (Pio@C-HA-DOs) for Osteoarthritis Treatment.International journal of nanomedicine · 2023Article
- The role of AGEs in pathogenesis of cartilage destruction in osteoarthritis.Bone & joint research · 2022Article
- Dendritic cell-mediated chronic low-grade inflammation is regulated by the RAGE-TLR4-PKCβMolecular medicine (Cambridge, Mass.) · 2022Article
- Crosstalk Between Senescent Bone Cells and the Bone Tissue Microenvironment Influences Bone Fragility During Chronological Age and in Diabetes.Frontiers in physiology · 2022Review
- Peroxisome Proliferator-Activated Receptor-Gamma (PPAR-ɣ): Molecular Effects and Its Importance as a Novel Therapeutic Target for Cerebral Ischemic Injury.Neurochemical research · 2021Review
- Betel Nut Chewing Decreased Calcaneus Ultrasound T-Score in a Large Taiwanese Population Follow-Up Study.Nutrients · 2021Article
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- Dieckol Attenuated Glucocorticoid-Induced Muscle Atrophy by Decreasing NLRP3 Inflammasome and Pyroptosis.International journal of molecular sciences · 2021Article
- Diabetes - osteoarthritis and joint pain.Bone & joint research · 2021Article
- Chondroprotective effects of purple corn anthocyanins on advanced glycation end products induction through suppression of NF-κB and MAPK signaling.Scientific reports · 2021Article
- Role of peroxisome proliferators-activated receptor-gamma in advanced glycation end product-mediated functional loss of voltage-gated potassium channel in rat coronary arteries.BMC cardiovascular disorders · 2020Article
Corrections and comments
- Retraction · 2024-05-01Concerns/Issues about Data · Concerns/Issues about Image · Concerns/Issues about Results and/or Conclusions · Duplication of Data · Duplication of/in Article · Duplication of/in Image · Euphemisms for Duplication · Investigation by Journal/Publisher · Original Data and/or Images not Provided and/or not Available · Unreliable Data · Unreliable Results and/or Conclusions ·
- Retracted
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Accumulation of advanced glycation end products (AGEs) in joints is important in the development of cartilage destruction and damage in age-related osteoarthritis (OA). The aim of this study was to investigate the roles of peroxisome proliferator-activated receptor γ (PPARγ), toll-like receptor 4 (TLR4), and receptor for AGEs (RAGE) in AGEs-induced inflammatory signalings in human OA chondrocytes. Human articular chondrocytes were isolated and cultured. The productions of metalloproteinase-13 and interleukin-6 were quantified using the specific ELISA kits. The expressions of related signaling proteins were determined by Western blotting. Our results showed that AGEs enhanced the productions of interleukin-6 and metalloproteinase-13 and the expressions of cyclooxygenase-2 and high-mobility group protein B1 and resulted in the reduction of collagen II expression in human OA chondrocytes. AGEs could also activate nuclear factor (NF)-κB activation. Stimulation of human OA chondrocytes with AGEs significantly induced the up-regulation of TLR4 and RAGE expressions and the down-regulation of PPARγ expression in a time- and concentration-dependent manner. Neutralizing antibodies of TLR4 and RAGE effectively reversed the AGEs-induced inflammatory signalings and PPARγ down-regulation. PPARγ agonist pioglitazone could also reverse the AGEs-increased inflammatory signalings. Specific inhibitors for p38 mitogen-activated protein kinases, c-Jun N-terminal kinase and NF-κB suppressed AGEs-induced PPARγ down-regulation and reduction of collagen II expression. Taken together, these findings suggest that AGEs induce PPARγ down-regulation-mediated inflammatory signalings and reduction of collagen II expression in human OA chondrocytes via TLR4 and RAGE, which may play a crucial role in the development of osteoarthritis pathogenesis induced by AGEs accumulation.
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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.