ReviewInternational journal of molecular sciences2023
Inflammatory and Metabolic Signaling Interfaces of the Hypertrophic and Senescent Chondrocyte Phenotypes Associated with Osteoarthritis.
Review in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers, 2 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
67 citing papers in PubMed, 2 syntheses or guidelines pooled it, 74 citations in OpenAlex.
- Bibliometric analysis of research trends and emerging insights of osteoarthritis and chondrocyte hypertrophy.Frontiers in surgery · 2025Pooled it
- A systematic review and meta-analysis of the efficacy and safety of iguratimod in the treatment of inflammatory arthritis and degenerative arthritis.Frontiers in pharmacology · 2024Pooled it
- Immune dysregulation in osteoarthritis: Mechanisms, biomarkers, and therapeutic opportunities.Journal of translational autoimmunity · 2026Review
- Critical role of Sirtuin 6 (SIRT6) in osteoarthritis chondrocytes: the interaction among various biological processes.Annals of medicine · 2026Review
- The regulatory significance of chondrocyte hypertrophy in maintaining chondrocyte homeostasis, regeneration and repair.Future science OA · 2026Review
- Single-cell RNA sequencing reveals chondrocyte heterogeneity and fibrocartilage transition in osteonecrosis of the femoral head.iScience · 2026Article
- Artificial mitochondria ameliorates osteoarthritis through restoring cellular energy metabolism homeostasis.Bioactive materials · 2026Article
- Exosomal LINC01106 From PRP-Treated ADSCs Alleviates Chondrocyte Inflammatory Injury by Sponging miR-34a-5p to Upregulate SIRT1 Expression.Cartilage · 2026Article
- CK2.1 Activates Chondrogenesis by Regulation of the p38 Mitogen-Activated Protein Kinase Pathway.Kinases and phosphatases · 2026Article
- Targeting TLR4/non-canonical NF-κB pathway by Bushen Bitong recipe enhances BMSCs-based cartilage repair in osteoarthritis.Biochemistry and biophysics reports · 2026Article
- Effects and mechanisms of synovial mesenchymal stem cell-derived extracellular vesicular LncRNA-SNHG14 on chondrocyte injury.Regenerative therapy · 2026Article
- YAP1 Knockdown Reduces IL-1β-Induced Human Chondrocyte Inflammation and Promotes Human MSC Chondrogenesis.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Dysregulation of the glycolysis-mitochondrial metabolism axis in osteoarthritis: mechanisms and therapeutic implications.Journal of orthopaedic translation · 2026Review
- Exploratory study of dialysis membrane impact on epigenetic methylation patterns in hemodialysis patients using genomic and synchrotron investigations.Scientific reports · 2026Article
- SHP2 suppressed the progression of IL-1β induced cartilage damage via modulating BRD4 associated autophagy and pyroptosis signaling pathway.Scientific reports · 2026Article
- Hsa_circ_0101645 contributes to excessive autophagy and apoptosis in intervertebral disc degeneration by acting as a miR-1304-5p sponge modulating BNIP3 expression.Non-coding RNA research · 2026Article
- Ectodysplasin-A (EDA) Signaling Cross-Talk in Skeletogenesis.Calcified tissue international · 2026Review
- Investigating Sex-Linked miRNAs for Potential Osteoarthritis Therapy Biomarkers.International journal of molecular sciences · 2026Article
- Molecular Mechanisms of Chondrocyte Hypertrophy Mediated by Physical Cues and Therapeutic Strategies in Osteoarthritis.International journal of molecular sciences · 2026Review
- Bioactive Phytoconstituents Targeting Energy Expenditure and Appetite to Combat Obesity: A Comprehensive Review.Current nutrition reports · 2026Review
7 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Osteoarthritis (OA) is a complex disease of whole joints with progressive cartilage matrix degradation and chondrocyte transformation. The inflammatory features of OA are reflected in increased synovial levels of IL-1β, IL-6 and VEGF, higher levels of TLR-4 binding plasma proteins and increased expression of IL-15, IL-18, IL-10 and Cox2, in cartilage. Chondrocytes in OA undergo hypertrophic and senescent transition; in these states, the expression of Sox-9, Acan and Col2a1 is suppressed, whereas the expression of RunX2, HIF-2α and MMP-13 is significantly increased. NF-kB, which triggers many pro-inflammatory cytokines, works with BMP, Wnt and HIF-2α to link hypertrophy and inflammation. Altered carbohydrate metabolism and the upregulation of GLUT-1 contribute to the formation of end-glycation products that trigger inflammation via the RAGE pathway. In addition, a glycolytic shift, increased rates of oxidative phosphorylation and mitochondrial dysfunction generate reactive oxygen species with deleterious effects. An important surveyor mechanism, the YAP/TAZ signaling system, controls chondrocyte differentiation, inhibits ageing by protecting the nuclear envelope and suppressing NF-kB, MMP-13 and aggrecanases. The inflammatory microenvironment and synthesis of key matrix components are also controlled by SIRT1 and mTORc. Senescent chondrocytes represent the functional end stage of hypertrophic differentiation and characteristically upregulate p16 and p21, but also a variety of inflammatory cytokines, chemokines and metalloproteinases, developing the senescence-associated secretory phenotype. Senolysis with dendrobin, miR29b-5p and other agents has been shown to be efficient under experimental conditions, and appears to be a promising tool for the treatment of OA, as it restores COL2A1 and aggrecan synthesis, suppressing NF-kB and destructive metalloproteinases.
Indexed as
Identifiers
What OpenQuestion holds
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.