ReviewNature reviews. Rheumatology2018
Mitochondrial DNA variation and the pathogenesis of osteoarthritis phenotypes.
Review in Nature reviews. Rheumatology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 103 papers, 2 of them syntheses 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
103 citing papers in PubMed, 2 syntheses or guidelines pooled it, 194 citations in OpenAlex.
- A meta-analysis and a functional study support the influence of mtDNA variant m.16519C on the risk of rapid progression of knee osteoarthritis.Annals of the rheumatic diseases · 2023Pooled it
- The pharmacological properties and corresponding mechanisms of farrerol: a comprehensive review.Pharmaceutical biology · 2022Pooled it
- Article
- 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
- Mesenchymal stromal cells therapy for remodeling the joint microenvironment: mechanisms, nanotechnology-enhanced strategies, and translation prospects.Stem cell research & therapy · 2026Review
- Research progress on cellular senescence in the pathogenesis and treatment of osteoarthritis and temporomandibular joint osteoarthritis.Journal of oral & facial pain and headache · 2026Review
- Targeting WWP1 ameliorates osteoarthritis by suppressing KLF15 ubiquitination to restore mtDNA and mitochondrial function.Molecular genetics and genomics : MGG · 2026Article
- Platinum nanozymes pursue cellular redox homeostasis: playing dual roles as pro-oxidants and antioxidants.Journal of nanobiotechnology · 2026Review
- Extracellular vesicles from IPFP-MSCs trigger osteoarthritis by transferring mtDNA.Bioactive materials · 2026Article
- The need to understand the underlying mechanisms associated with mitochondrial therapies in assisted reproduction before further clinical trials are performed.Human reproduction (Oxford, England) · 2026Review
- Targeted knockdown of Piezo1 in synovial macrophages attenuates osteoarthritis development.Journal of orthopaedic translation · 2026Article
- Targeting the mitochondrial metabolite-dynamics-MDVs-MitoEVs axis: a new frontier in osteoarthritis management.Journal of translational medicine · 2026Review
- Mechanism driven adaptation of smart hydrogels to the osteoarthritis pathological microenvironment.Frontiers in bioengineering and biotechnology · 2026Review
- Revisiting osteoarthritis pathogenesis through the lens of cGAS-STING: Mitochondrial damage, pyroptosis, and inflammatory cascades.Journal of orthopaedic translation · 2026Review
- A Comprehensive Reactive-Oxygen-Species-Scavenging Metal-Organic Framework Orchestrates the AMPK-DOT1L-H3K79me3 Cascade to Alleviate Osteoarthritis.Biomaterials research · 2026Article
- Spontaneous hydrogen-releasing nanoenzyme alleviates osteoarthritis via oxidative stress reduction and mitochondrial dysfunction reversal.Journal of nanobiotechnology · 2025Article
- Relationship between RAR and the risk of osteoarthritis: a comprehensive analysis based on NHANES data (1999-2018).Journal of orthopaedics · 2025Article
- High-mobility network hydrogel microsphere system to combat chondrocyte senescence for enhanced cartilage repair and regeneration.Materials today. Bio · 2025Article
- Therapeutic restoration of mitochondria-endoplasmic reticulum cross talk for osteoarthritis.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
43 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 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondria and mitochondrial DNA (mtDNA) variation are now recognized as important factors in the development of osteoarthritis (OA). Mitochondria are the energy powerhouses of the cell, and also regulate different processes involved in the pathogenesis of OA including inflammation, apoptosis, calcium metabolism and the generation of reactive oxygen species (ROS) and reactive nitrogen species (RNS). Mitochondria contain their own genetic material, mtDNA, which evolved through the sequential accumulation of mtDNA variants to enable humans to adapt to different climates. The ROS and reactive metabolic intermediates that are by-products of mitochondrial metabolism are regulated in part by mtDNA and are among the signals that transmit information between mitochondria and the nucleus. These signals can alter nuclear gene expression and, when disrupted, affect a number of cellular processes and metabolic pathways, leading to disease. mtDNA variation influences OA-associated phenotypes, including those related to metabolism, inflammation and even ageing, as well as nuclear epigenetic regulation. This influence also enables the use of specific mtDNA haplogroups as complementary diagnostic and prognostic biomarkers of OA.
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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.