ArticleJournal of clinical medicine2019
Pink1-Mediated Chondrocytic Mitophagy Contributes to Cartilage Degeneration in Osteoarthritis.
Article in Journal of clinical medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.
What it found
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The trial behind it
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Who cites it
59 citing papers in PubMed, 83 citations in OpenAlex.
- Repetitive Compressive Loading Downregulates the Expression of Autophagy-Related Factors, Autophagy Capacity and Cellular Activity in Human Osteoarthritic Chondrocytes.International journal of molecular sciences · 2026Article
- The role of the HB-EGF-regulated EGFR-mitophagy axis in maintaining cartilage homeostasis and osteoarthritis.Journal of molecular histology · 2026Article
- Exploring mitochondrial functions and dysfunctions in chondrocytes: toward the identification of novel therapies for osteoarthritis.Bone research · 2026Review
- USP34 attenuates cartilage degradation in temporomandibular joint osteoarthritis by ANT1-mediated mitophagy.JBMR plus · 2026Article
- Chondrocyte Senescence in Osteoarthritis: Potential Targets and Pharmacological Interventions.Cartilage · 2026Article
- Targeting mitochondrial quality control in osteoarthritis with GrpE-like 1-loaded synovial mesenchymal stromal/stem cell small extracellular vesicles.World journal of stem cells · 2026Article
- LOXL2 deletion triggers TMJ osteoarthritis, while overexpression protects it from NF-κB-induced chondrocyte apoptosis.International journal of oral science · 2026Article
- Targeting the mitochondrial metabolite-dynamics-MDVs-MitoEVs axis: a new frontier in osteoarthritis management.Journal of translational medicine · 2026Review
- Mitochondrial-targeted therapy for osteoarthritis: Challenges and opportunities from basic research to clinical translation.Frontiers in immunology · 2026Review
- Traditional Chinese medicine-derived monomers delay osteoarthritis progression by regulating mitochondrial homeostasis.Frontiers in cell and developmental biology · 2026Review
- The osteoarthritis inflammatory ecosystem: a node-edge-boundary-emergent framework toward precision stratification and therapeutic hypothesis generation.Frontiers in medicine · 2026Review
- PINK1 overexpression suppresses p38 MAPK/NF‑κB signaling to attenuate chondrocyte senescence in osteoarthritis.International journal of molecular medicine · 2025Article
- Engineered exosomal miR140 modulates mitophagy of chondrocytes through targeting CAPN1 to alleviate osteoarthritis.Science China. Life sciences · 2025Article
- The impact of mitochondrial dysfunction on osteoarthritis cartilage: current insights and emerging mitochondria-targeted therapies.Bone research · 2025Review
- Dehydrotanshinone II A alleviates osteoarthritis via activating PPARγ to inhibit ferroptosis in chondrocytes.Scientific reports · 2025Article
- A Molecular Chemical Perspective: Mitochondrial Dynamics Is Not a Bystander of Cartilage Diseases.ACS pharmacology & translational science · 2025Review
- SIRT3-PINK1-PKM2 axis prevents osteoarthritis via mitochondrial renewal and metabolic switch.Bone research · 2025Article
- The inhibition of PINK1/Drp1-mediated mitophagy by hyperglycemia leads to impaired osteoblastogenesis in diabetes.iScience · 2025Article
- Fasting activates optineurin-mediated mitophagy in chondrocytes to protect against osteoarthritis.Communications biology · 2025Article
- AM1241 inhibits chondrocyte inflammation and ECM degradation through the Nrf2/HO-1 and NF-κB pathways and alleviates osteoarthritis in mice.Molecular medicine (Cambridge, Mass.) · 2025Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
Abstract
Cartilage loss is a central event in the pathogenesis of osteoarthritis (OA), though other than mechanical loading, the biochemical mechanisms underlying OA pathology remain poorly elucidated. We investigated the role of Pink1-mediated mitophagy in mitochondrial fission, a crucial process in OA pathogenesis. We used a monosodium iodoacetate (MIA)-induced rodent model of OA, which inhibits the activity of articular chondrocytes, leading to disruption of glycolytic energy metabolism and eventual cell death. The OA rat cartilage exhibits significant induction of autophagy-related proteins LC3B and p62, similar to human osteoarthritic cartilage. Moreover, expression of Pink1 and Parkin proteins were also increased in OA. Here, we confirm that Pink1-mediated mitophagy leads to cell death in chondrocytes following MIA treatment, while deficiency in Pink1 expression was associated with decreased cartilage damage and pain behaviors in MIA-induced OA. Finally, we found that autophagy and mitophagy-related genes are highly expressed in human osteoarthritic cartilage. These results indicate that OA is a degenerative condition associated with mitophagy, and suggest that targeting the Pink1 pathway may provide a therapeutic avenue for OA treatment.
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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.