ReviewNature reviews. Rheumatology2011
The role of mitochondria in osteoarthritis.
Review in Nature reviews. Rheumatology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 294 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
294 citing papers in PubMed, 1 synthesis or guideline pooled it, 537 citations in OpenAlex.
- Lycium barbarum polysaccharides in ageing and its potential use for prevention and treatment of osteoarthritis: a systematic review.BMC complementary medicine and therapies · 2021Pooled it
- Trial
- Molecular hydrogen and osteoarthritis: multi-target mechanisms and therapeutic effectiveness.Medical gas research · 2027Review
- Acute TGFα drives OA-associated transcriptional and metabolic remodelling in primary chondrocytes.Osteoarthritis and cartilage open · 2026Article
- Article
- From Joint Loading to Osteoarthritis: A Multiscale Review of Knee Mechanobiology and Digital Modelling.International journal of molecular sciences · 2026Review
- Metabolic disorders and osteoarthritis: novel insights into pathological mechanisms and therapeutic strategies.Life medicine · 2026Review
- Article
- The Effect of Physical, Biochemical, and Electrical Culture Conditions on Articular Chondrocytes Used for Cartilage Tissue Engineering: A Narrative Review.International journal of molecular sciences · 2026Review
- GPNMBCell reports. Medicine · 2026Article
- Restoring Metabolic-Inflammatory Homeostasis: Curcumin's Multi-Layered Defense Against Chondrocyte Dysfunction.Metabolites · 2026Article
- Therapeutic effect of mitochondrial transfer on bone tissue diseases: treatment strategy of mitochondrial transplantation and delivery technology.Journal of orthopaedic translation · 2026Review
- Mitochondrial dysfunction activates ADAMTS-5 expression via mt-dsRNA-PKR-Spi-1 axis in osteoarthritic chondrocytes.iScience · 2026Article
- Aptamer-functionalized apoptotic vesicles ameliorate osteoarthritis via resuming mitochondria OXPHOS of chondrocytes.Science advances · 2026Article
- Exploring mitochondrial functions and dysfunctions in chondrocytes: toward the identification of novel therapies for osteoarthritis.Bone research · 2026Review
- Next-generation therapies for osteoarthritis: the evolving role of cell therapy products.Experimental & molecular medicine · 2026Review
- Microfluidic methacrylated hyaluronic acid microspheres incorporating MnOMaterials today. Bio · 2026Article
- Cellular Products with Anti-Inflammatory Properties for the Treatment of Cartilage Lesions.International journal of molecular sciences · 2026Review
- Vertebral BMSC-EVs under estrogen deficiency drive senescence-related mitochondrial dysfunction in endplate chondrocytes via MRPL1 mRNA delivery.Experimental & molecular medicine · 2026Article
- Interleukin-1 Receptor-Associated Kinase 3 Attenuates Chondrocyte Senescence and Osteoarthritis via Inhibition of the TLR7/9-NF-κB Axis.Journal of molecular histology · 2026Article
234 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
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondria are important regulators of cellular function and survival that may have a key role in aging-related diseases. Mitochondrial DNA (mtDNA) mutations and oxidative stresses are known to contribute to aging-related changes. Osteoarthritis (OA) is an aging-associated rheumatic disease characterized by articular cartilage degradation and elevated chondrocyte mortality. Articular cartilage chondrocytes survive and maintain tissue integrity in an avascular, low-oxygen environment. Recent ex vivo studies have reported mitochondrial dysfunction in human OA chondrocytes, and analyses of mitochondrial electron transport chain activity in these cells show decreased activity of Complexes I, II and III compared to normal chondrocytes. This mitochondrial dysfunction may affect several pathways that have been implicated in cartilage degradation, including oxidative stress, defective chondrocyte biosynthesis and growth responses, increased cytokine-induced chondrocyte inflammation and matrix catabolism, cartilage matrix calcification, and increased chondrocyte apoptosis. Mitochondrial dysfunction in OA chondrocytes may derive from somatic mutations in the mtDNA or from the direct effects of proinflammatory mediators such as cytokines, prostaglandins, reactive oxygen species and nitric oxide. Polymorphisms in mtDNA may become useful as biomarkers for the diagnosis and prognosis of OA, and modulation of serum biomarkers by mtDNA haplogroups supports the concept that mtDNA haplogroups may define specific OA phenotypes in the complex OA process.
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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.