ArticleCartilage2021
Hypoxia Inducible Factor-1α Is a Regulator of Autophagy in Osteoarthritic Chondrocytes.
Article in Cartilage, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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
26 citing papers in PubMed, 30 citations in OpenAlex.
- HIF-PH Inhibitor Promotes Stabilization of HIF-1α via Inhibition of Its Degradation and Exerts Chondroprotective Effects in a Rat Osteoarthritis Model.International journal of molecular sciences · 2026Article
- Exploring the potential application of roxadustat in chronic kidney disease-related osteoporosis based on the regulatory role of HIF-1α in bone metabolism.Histology and histopathology · 2026Review
- Mitochondrial homeostasis in bone aging: Unraveling dysfunctional pathways and developing precision therapies.Fundamental research · 2026Review
- Programmed cell death in osteoarthritis.Apoptosis : an international journal on programmed cell death · 2026Review
- Hypoxia-Inducible Factors in Rheumatoid Arthritis: Central Pathogenic Roles and Therapeutic Opportunities.Journal of inflammation research · 2026Review
- HIF-1α-centered metabolic reprogramming in osteoarthritis: cell type-specific effects and intercellular crosstalk among chondrocytes, BMSCs, and macrophages.Frontiers in immunology · 2026Review
- The dual role of autophagy in cartilage degradation: from mechanisms to targeted therapeutics.Frontiers in cell and developmental biology · 2026Review
- Interplay between ALK2Cell death discovery · 2025Article
- Fasting activates optineurin-mediated mitophagy in chondrocytes to protect against osteoarthritis.Communications biology · 2025Article
- Programmed Cell Death of Chondrocytes, Synovial Cells, Osteoclasts, and Subchondral Bone Cells in Osteoarthritis.Journal of inflammation research · 2025Review
- Article
- New insights into the mechanisms and therapeutic strategies of chondrocyte autophagy in osteoarthritis.Journal of molecular medicine (Berlin, Germany) · 2024Review
- Cartilage Homeostasis under Physioxia.International journal of molecular sciences · 2024Review
- Advances in the study of mitophagy in osteoarthritis.Journal of Zhejiang University. Science. B · 2024Article
- LncRNAs as nodes for the cross-talk between autophagy and Wnt signaling in pancreatic cancer drug resistance.International journal of biological sciences · 2024Review
- Bioinformatics identification and integrative analysis of ferroptosis-related key lncRNAs in patients with osteoarthritis.Bioscience reports · 2023Article
- ZnO Nanorods Create a Hypoxic State with Induction of HIF-1 and EPAS1, Autophagy, and Mitophagy in Cancer and Non-Cancer Cells.International journal of molecular sciences · 2023Article
- Osteoarthritis: pathogenic signaling pathways and therapeutic targets.Signal transduction and targeted therapy · 2023Review
- Regulatory mechanisms of autophagy-related ncRNAs in bone metabolic diseases.Frontiers in pharmacology · 2023Review
- Glycolysis: an emerging regulator of osteoarthritis.Frontiers in immunology · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveTo investigate the relationship between hypoxia inducible factor-1α (HIF-1α) and the autophagic response in osteoarthritic chondrocytes (OA), under inflammatory insult as represented by
methodsHuman chondrocyte cell line C28/I2 was cultured in both normoxic and hypoxic conditions and treated with interleukin-1β (IL1β) to emulate OA inflammatory insult
resultsChondrocyte basal autophagy levels were higher in a HIF-1α elevated environment and was more resistant to IL1β-induced inflammatory insult. Increase in autophagic proteins showed better chondrocyte repair, which resulted a lower level of reactive oxygen species production, and lesser damage to chondrocyte integrity. Silencing HIF-1α activates cellular PINK1/Parkin and BNIP3 mitophagic proteins, which leads to the activation of Caspase/Cleaved Caspase 3 apoptotic cascade.
conclusionOur results show that chondrocyte autophagy is dependent on HIF-1α expression, showing the importance of HIF-1α in hypoxic chondrocyte function in OA. Dysregulation of HIF-1α expression results in the activation of mitophagy-mediated apoptosis.
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.