ArticleNature communications2025
Mitochondria relay cholesterol signal exacerbates osteoarthritis in mice.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.
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Who cites it
8 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Mitochondria transfer research from cellular mechanisms to immune-inflammatory and translational frontiers: a bibliometric analysis from 2006 to 2026.Frontiers in immunology · 2026Pooled it
- Mitochondrial Communication Networks in the Bone Microenvironment: From the Maintenance of Homeostasis to Translational Interventions for Bone Diseases.Stem cell reviews and reports · 2026Review
- Osteocyte-vascular Interactions in Bone Physiology and Pathology.Current osteoporosis reports · 2026Review
- Intravital Depletion of Cholesterol Reduces Membrane Dynamics and Increases Mechanosensitivity in Osteocytes In Vivo.bioRxiv : the preprint server for biology · 2026Article
- Mitochondrial Transport in Bone Metabolism Homeostasis: Molecular Mechanisms and Targeted Therapeutic Strategies.International journal of molecular sciences · 2026Review
- Exploring mitochondrial functions and dysfunctions in chondrocytes: toward the identification of novel therapies for osteoarthritis.Bone research · 2026Review
- Cellular Products with Anti-Inflammatory Properties for the Treatment of Cartilage Lesions.International journal of molecular sciences · 2026Review
- DHCR24 Deficiency Drives Age-Related Meibomian Gland Dysfunction by Regulating Lipid Metabolic Imbalance and Cytosolic mtDNA-Induced cGAS-STING Activation.International journal of biological sciences · 2026Article
Corrections and comments
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Authors and funding
20 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Osteoarthritis (OA) is the most common joint disease characterized by joint inflammation and cartilage deterioration. Though disrupted cholesterol metabolism has been implicated in the pathogenesis of OA, the underlying mechanisms remains unclear. Here we demonstrate that increased cholesterol in joint is a crucial activator of the cGAS-STING pathway in cartilage during OA. Subchondral osteocytes, which contact with blood vessel and cartilage, increase their uptake of cholesterol and transfer mitochondria to cartilage to trigger its inflammatory pathway. This process is mediated by increased cytosolic mitochondrial DNA (mtDNA) in chondrocytes, and is further amplified through enhanced mitochondrial transfer between chondrocytes. Mechanistically, we identify a mitochondrial subpopulation in osteocytes that enriched in Nudt8, which act as a key regulator of metabolic-inflammatory crosstalk. Nudt8 alters cholesterol metabolism by degrading coenzyme A, leading to an accumulation of cytosolic mtDNA and subsequent activation of the cGAS-STING pathway in chondrocytes. Pharmacological targeting osteocyte mitochondrial Nudt8 by supplementing pantethine ameliorate inflammation in cartilage and joint pain in OA mice, offering a potential therapeutic strategy for 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.