ArticleOsteoarthritis and cartilage2009
Diminished mitochondrial DNA integrity and repair capacity in OA chondrocytes.
Article in Osteoarthritis and cartilage, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers, 3 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.
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Who cites it
71 citing papers in PubMed, 3 syntheses or guidelines pooled it, 139 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
- Single-dose local anesthetics exhibit a type-, dose-, and time-dependent chondrotoxic effect on chondrocytes and cartilage: a systematic review of the current literature.Knee surgery, sports traumatology, arthroscopy : official journal of the ESSKA · 2018Pooled it
- Role of mtDNA haplogroups in the prevalence of osteoarthritis in different geographic populations: a meta-analysis.PloS one · 2014Pooled it
- Exploring mitochondrial functions and dysfunctions in chondrocytes: toward the identification of novel therapies for osteoarthritis.Bone research · 2026Review
- Dysregulation of the glycolysis-mitochondrial metabolism axis in osteoarthritis: mechanisms and therapeutic implications.Journal of orthopaedic translation · 2026Review
- Mitochondrial transplantation for osteoarthritis: from molecular mechanisms to clinical translation.Frontiers in immunology · 2026Review
- Daphnetin-mediated mitophagy alleviates intervertebral disc degeneration via the Nrf2/PINK1 pathway.Acta biochimica et biophysica Sinica · 2025Article
- Heat-KilledNutrients · 2024Article
- Targeting PAR2-mediated inflammation in osteoarthritis: a comprehensive in vitro evaluation of oleocanthal's potential as a functional food intervention for chondrocyte protection and anti-inflammatory effects.BMC musculoskeletal disorders · 2024Article
- Engineering extracellular vesicles for ROS scavenging and tissue regeneration.Nano convergence · 2024Review
- The current insights of mitochondrial hormesis in the occurrence and treatment of bone and cartilage degeneration.Biological research · 2024Review
- Protective Effect of Knee Postoperative Fluid on Oxidative-Induced Damage in Human Knee Articular Chondrocytes.Antioxidants (Basel, Switzerland) · 2024Article
- Characterizing mitochondrial features in osteoarthritis through integrative multi-omics and machine learning analysis.Frontiers in immunology · 2024Article
- Antioxidant hydrogels for the treatment of osteoarthritis: mechanisms and recent advances.Frontiers in pharmacology · 2024Review
- The metabolic characteristics and changes of chondrocytesFrontiers in endocrinology · 2024Review
- Oxidative stress as a key modulator of cell fate decision in osteoarthritis and osteoporosis: a narrative review.Cellular & molecular biology letters · 2023Review
- Apoptosis Regulation in Osteoarthritis and the Influence of Lipid Interactions.International journal of molecular sciences · 2023Review
- How are Aging and Osteoarthritis Related?Aging and disease · 2023Review
- Mitochondrial Transfer as a Novel Therapeutic Approach in Disease Diagnosis and Treatment.International journal of molecular sciences · 2023Review
- An Integrated View of Stressors as Causative Agents in OA Pathogenesis.Biomolecules · 2023Review
11 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
4 authors at 1 institution in 1 country.
Funding
Abstract
objectivesOsteoarthritis (OA) is characterized by the failure of chondrocytes to respond to injury and perform the cartilage remodeling process. Human articular chondrocytes actively produce reactive oxygen and nitrogen species (ROS and RNS) capable of causing cellular dysfunction and death. A growing body of evidence indicates that mitochondrial dysfunction and mitochondrial DNA (mtDNA) damage play a causal role in disorders linked to excessive generation of oxygen free radicals. The aim of this study was to determine whether mtDNA damage was present in OA chondrocytes, and whether mtDNA repair capacity is compromised in OA chondrocytes following oxidative stress, leading to chondrocyte death.
methodsHuman articular cartilage was isolated from knee joints of cadavers available through the Anatomical Gifts Program at the University of South Alabama (normal donors) or OA patients undergoing total knee replacement surgeries (OA patients). Total DNA was isolated from either chondrocytes released following collagenase digestion, or from first passage chondrocytes grown in culture and exposed to ROS or RNS. mtDNA integrity and repair capacity were analyzed by quantitative Southern blot analysis, using a mtDNA-specific radioactive probe. Cell viability was determined by the trypan blue exclusion method.
resultsmtDNA damage was found in chondrocytes from OA patients compared to normal donors. It was accompanied with reduced mtDNA repair capacity, cell viability, and increased apoptosis in OA chondrocytes following exposure to ROS and RNS.
conclusionsThese results indicate that mtDNA damage and poor mtDNA repair capacity for removing damage caused by oxidative stress may contribute to the pathogenesis 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.