ReviewInternational journal of molecular sciences2024
Cartilage Homeostasis under Physioxia.
Review in International journal of molecular sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.
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.
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
15 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Prevalence of knee osteoarthritis in the Chinese population, 2013-2023: a systematic review and meta-analysis.Journal of orthopaedic surgery and research · 2025Pooled it
- Review
- Effects of the space environment on articular cartilage homeostasis: a review.NPJ microgravity · 2026Review
- Fibronectin Peptide FNIII14 Enhances Progressive Cartilage Degeneration in Osteoarthritis by Inducing Chondrocyte Apoptosis.Current issues in molecular biology · 2026Article
- State-of-the-Art and Next Generation Intra-Articular Implantable Biosensors for Osteoarthritis: From Analytical Limits to Operational Stability.Biosensors · 2026Review
- Effect of HIF-1α inhibitor LW6 on chondrogenic properties of mesenchymal stromal cells and chondrocytes in cell sheets under physioxia.Journal of biological engineering · 2026Article
- Lactate-driven lactylation reprograms chondrocyte fate and joint inflammation in osteoarthritis: linking metabolism with epigenetic regulation.Frontiers in cell and developmental biology · 2026Review
- LOXL1, THY1, and TYMS define an annotation-derived hemoglobin-associated immunotranscriptomic signature in osteoarthritis cartilage.Frontiers in immunology · 2026Article
- HIF-1α-centered metabolic reprogramming in osteoarthritis: cell type-specific effects and intercellular crosstalk among chondrocytes, BMSCs, and macrophages.Frontiers in immunology · 2026Review
- Exploring Endoplasmic Reticulum Stress-Related Genes in Cartilage Defects: Implications for Diagnosis and Therapy.Combinatorial chemistry & high throughput screening · 2026Article
- Current cutting-edge omics techniques on musculoskeletal tissues and diseases.Bone research · 2025Review
- Single BMSC-derived cartilage organoids for gradient heterogeneous osteochondral regeneration by leveraging native vascular microenvironment.Journal of nanobiotechnology · 2025Article
- Article
- Regulation of apoptosis and interaction with cartilage degeneration in osteoarthritis.Frontiers in cell and developmental biology · 2025Review
- Future perspectives: advances in bone/cartilage organoid technology and clinical potential.Biomaterials translational · 2024Review
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Articular cartilage receives nutrients and oxygen from the synovial fluid to maintain homeostasis. However, compared to tissues with abundant blood flow, articular cartilage is exposed to a hypoxic environment (i.e., physioxia) and has an enhanced hypoxic stress response. Hypoxia-inducible factors (HIFs) play a pivotal role in this physioxic environment. In normoxic conditions, HIFs are downregulated, whereas in physioxic conditions, they are upregulated. The HIF-α family comprises three members: HIF-1α, HIF-2α, and HIF-3α. Each member has a distinct function in articular cartilage. In osteoarthritis, which is primarily caused by degeneration of articular cartilage, HIF-1α is upregulated in chondrocytes and is believed to protect articular cartilage by acting anabolically on it. Conversely, in contrast to HIF-1α, HIF-2α exerts a catabolic influence on articular cartilage. It may therefore be possible to develop a new treatment for OA by controlling the expression of HIF-1α and HIF-2α with drugs or by altering the oxygen environment in the joints.
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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.