ArticleCell metabolism2014
Mitochondrial complex I activity suppresses inflammation and enhances bone resorption by shifting macrophage-osteoclast polarization.
Article in Cell metabolism, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05483738 (The Impact of Mitochondrial Dysfunction on Human Bone Cell Metabolism and Remodelling), which is not on this map. Cited by 177 papers.
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.
The Impact of Mitochondrial Dysfunction on Human Bone Cell Metabolism and Remodelling
Who cites it
177 citing papers in PubMed, 273 citations in OpenAlex.
- Nitric oxide modulates bone anabolism through regulation of osteoblast glycolysis and differentiation.The Journal of clinical investigation · 2021Trial
- Thromboxane A2 receptor signalling amplifies osteoclastogenesis in rheumatoid arthritis through ACSL1 associated mitochondrial oxidative metabolism.Nature communications · 2026Article
- Convergent mitochondrial impairment and apoptosis driven by simultaneous down-regulation of multiple genes at 11p11.2 in Alzheimer's disease.Molecular psychiatry · 2026Article
- Hierarchical Nanoplatform Integrating Oxidative-Acidic Microenvironment Remodeling and Bone Homeostasis Modulation for Diabetic Bone Defect Therapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Mitochondrial OXPHOS integrates immunometabolic cascade for bone regeneration via coupled ATP production and ROS homeostasis.Redox biology · 2026Article
- Paeonol and Its Metabolites Alleviate LPS/D-GalN-Induced Acute Liver Injury in Mice: Potential Involvement of NDUFS7 and Macrophage Mitochondrial Function.Antioxidants (Basel, Switzerland) · 2026Article
- Comorbidities and Inflammation: How Chronic Diseases Prime the Host Response in Sepsis.International journal of molecular sciences · 2026Review
- The NLRP12 Osteoimmune Checkpoint: Coordinating Inflammatory Signaling and Bone Remodeling.Biomedicines · 2026Review
- Promoting Bone Health in Layer Chickens from the Perspective of Mitochondrial Energy Metabolism in Osteoclasts.Animals : an open access journal from MDPI · 2026Review
- Metformin as a Metabolic Reprogramming Interface in Host-Pathogen and Bone Microenvironment Crosstalk: A Dual-Target Strategy Against Antimicrobial Resistance and Osteoporotic Bone Loss.Antibiotics (Basel, Switzerland) · 2026Review
- Novel Organelle-Based Intracellular Immunity with Mechanistic and Therapeutic Implications.Barrier immunity · 2026Article
- Mitochondrial homeostasis in bone aging: Unraveling dysfunctional pathways and developing precision therapies.Fundamental research · 2026Review
- Hells protects mitochondrial integrity via Nr2f2 suppression during osteoclast differentiation.Cell communication and signaling : CCS · 2026Article
- Synthetic Novel Flavonoids SZQ-4 Suppress Osteoclastogenesis and Ameliorate Osteoporosis via Inhibiting Reactive Oxygen Species and Regulating SIRT3.Antioxidants (Basel, Switzerland) · 2026Article
- Osteoblast-derived osteomodulin restrains osteoclastogenesis via ITGB8/RRM2-mediated reduction of mitochondrial respiration and mitochondrial ATP production.Experimental & molecular medicine · 2026Article
- Inflammation Affects the Osteogenic Differentiation of Aged Periodontal Ligament Cells via NF-κB/FOXO3a/c-JUN Signalling.Journal of periodontal research · 2026Article
- Pioglitazone Ameliorates Mitochondrial Oxidative Stress and Inflammation via AMPK-Dependent Inhibition of Mitochondrial Fission in Leigh Syndrome.Cell proliferation · 2026Article
- Leigh Syndrome Pathomechanism Involves Region-Specific Innate Immune Activation in Ndufs4 Knockout Mice.Cellular and molecular neurobiology · 2026Article
- Mitochondrial complex I in focus: mechanisms and therapeutic strategies of urinary system diseases.Frontiers in physiology · 2026Review
- Mitochondrial regulation of stem cell osteogenic differentiation: A key driver for bone regeneration.World journal of stem cells · 2025Article
117 more citing papers are in PubMed but not listed here.
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Mitochondrial complex I (CI) deficiency is associated with multiple neurological and metabolic disorders. However, its effect on innate immunity and bone remodeling is unclear. Using deletion of the essential CI subunit Ndufs4 as a model for mitochondrial dysfunction, we report that mitochondria suppress macrophage activation and inflammation while promoting osteoclast differentiation and bone resorption via both cell-autonomous and systemic regulation. Global Ndufs4 deletion causes systemic inflammation and osteopetrosis. Hematopoietic Ndufs4 deletion causes an intrinsic lineage shift from osteoclast to macrophage. Liver Ndufs4 deletion causes a metabolic shift from fatty acid oxidation to glycolysis, accumulating fatty acids and lactate (FA/LAC) in the circulation. FA/LAC further activates Ndufs4(-/-) macrophages via reactive oxygen species induction and diminishes osteoclast lineage commitment in Ndufs4(-/-) progenitors; both inflammation and osteopetrosis in Ndufs4(-/-) mice are attenuated by TLR4/2 deletion. Together, these findings reveal mitochondrial CI as a critical rheostat of innate immunity and skeletal homeostasis.
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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.