ArticleJournal of cell science2020
Mitochondrial dysfunction triggers a catabolic response in chondrocytes via ROS-mediated activation of the JNK/AP1 pathway.
Article in Journal of cell science, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 44 citations in OpenAlex.
- Acute TGFα drives OA-associated transcriptional and metabolic remodelling in primary chondrocytes.Osteoarthritis and cartilage open · 2026Article
- Piezo1 accelerates osteoarthritis progression via promotion of HBB-dependent oxidative phosphorylation.The Journal of biological chemistry · 2026Article
- Mitochondrial dysfunction activates ADAMTS-5 expression via mt-dsRNA-PKR-Spi-1 axis in osteoarthritic chondrocytes.iScience · 2026Article
- High-throughput histopathology for complex in vitro models.Cell reports methods · 2026Article
- Loss of connexin 43 in cartilage causes mitochondrial dysfunction and accelerates post-traumatic osteoarthritis progression.bioRxiv : the preprint server for biology · 2026Article
- Stress-activated pathways mediate PFAS effects on human placental syncytiotrophoblast cells.Toxicological sciences : an official journal of the Society of Toxicology · 2026Article
- Exploring mitochondrial functions and dysfunctions in chondrocytes: toward the identification of novel therapies for osteoarthritis.Bone research · 2026Review
- Oxygen tension alters cartilage redox balance in response to traumatic impact.Bone & joint research · 2026Article
- Targeting mitochondrial oxidative stress: A novel therapeutic strategy for degenerative joint diseases (Review).Biomedical reports · 2026Review
- Energy crisis and cartilage collapse: metabolic reprogramming of chondrocytes in osteoarthritis.Frontiers in immunology · 2026Review
- Transcriptome-based profiling of programmed cell death signatures identifies two osteoarthritis subtypes and the hub gene DNM1L.Frontiers in immunology · 2026Article
- High-Resolution 3-Dimensional Micro-CT Imaging of Intervertebral Discs Using a Novel Contrast Agent.JOR spine · 2025Article
- Mechanical Stimulation of Equine Bone Marrow Mesenchymal Stromal Cell-Derived Cartilage-Like In Vitro Model Triggers Osteoarthritis Features.ACS biomaterials science & engineering · 2025Article
- Proteomic analysis of hydrogen peroxide-treated human chondrocytes shows endoplasmic reticulum stress, cytoskeleton remodeling, and altered secretome composition.Cell communication and signaling : CCS · 2025Article
- Loosening the Lid on Shoulder Osteoarthritis: How the Transcriptome and Metabolic Syndrome Correlate with End-Stage Disease.International journal of molecular sciences · 2025Article
- Upregulation of CD244 promotes CD8Parasites & vectors · 2024Article
- Bats as instructive animal models for studying longevity and aging.Annals of the New York Academy of Sciences · 2024Review
- PANX1-mediated ATP release confers FAM3A's suppression effects on hepatic gluconeogenesis and lipogenesis.Military Medical Research · 2024Article
- The metabolic characteristics and changes of chondrocytesFrontiers in endocrinology · 2024Review
- Regulation of ferroptosis in osteoarthritis and osteoarthritic chondrocytes by typical MicroRNAs in chondrocytes.Frontiers in medicine · 2024Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Mitochondrial function is impaired in osteoarthritis (OA) but its impact on cartilage catabolism is not fully understood. Here, we investigated the molecular mechanism of mitochondrial dysfunction-induced activation of the catabolic response in chondrocytes. Using cartilage slices from normal and OA cartilage, we showed that mitochondrial membrane potential was lower in OA cartilage, and that this was associated with increased production of mitochondrial superoxide and catabolic genes [interleukin 6 (IL-6), COX-2 (also known as PTGS2), MMP-3, -9, -13 and ADAMTS5]. Pharmacological induction of mitochondrial dysfunction in chondrocytes and cartilage explants using carbonyl cyanide 3-chlorophenylhydrazone increased mitochondrial superoxide production and the expression of IL-6, COX-2, MMP-3, -9, -13 and ADAMTS5, and cartilage matrix degradation. Mitochondrial dysfunction-induced expression of catabolic genes was dependent on the JNK (herein referring to the JNK family)/activator protein 1 (AP1) pathway but not the NFκB pathway. Scavenging of mitochondrial superoxide with MitoTEMPO, or pharmacological inhibition of JNK or cFos and cJun, blocked the mitochondrial dysfunction-induced expression of the catabolic genes in chondrocytes. We demonstrate here that mitochondrial dysfunction contributes to OA pathogenesis via JNK/AP1-mediated expression of catabolic genes. Our data shows that AP1 could be used as a therapeutic target for OA management.This article has an associated First Person interview with the first author of the paper.
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