ArticlePloS one2016
Accelerated Lactate Dehydrogenase Activity Potentiates Osteoclastogenesis via NFATc1 Signaling.
Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed, 57 citations in OpenAlex.
- Glycolysis in bone remodeling: from energy supply to signaling regulation.Molecular biology reports · 2026Review
- A novelLife science alliance · 2026Article
- Histone H3K18 lactylation: An exercise-induced epigenetic mechanism that inhibits osteoclast activity and protects against osteoporosis.Journal of orthopaedic translation · 2026Article
- The emerging role of lactate in skeletal homeostasis and disorders: Integrated mechanisms and translational opportunities.Journal of orthopaedic translation · 2026Review
- Lactate and lactylation in osteoporosis: pathogenesis, regulation, and future perspectives.Journal of bone and mineral metabolism · 2026Review
- The role of lactate on arthritis-associated cells: physiology, pathology, and therapeutic strategies.Cellular and molecular life sciences : CMLS · 2026Review
- Bone Marrow Immunometabolic Remodeling in Osteoporosis: From Systemic Risk Factors to Precision Intervention.International journal of general medicine · 2026Review
- Multi-system Mechanisms in the Anti-osteoporotic Effects of Herbal Natural Products.Endocrine, metabolic & immune disorders drug targets · 2026Review
- Protein succinylome analysis identifies citrate synthase as a central regulator of osteoclast metabolic activity.The FEBS journal · 2025Article
- Mechanisms and therapeutic perspectives of mitochondrial dysfunction of macrophages in periodontitis.Frontiers in cellular and infection microbiology · 2025Review
- Macrophages in osteoporotic fractures: from immunometabolic mechanisms to precision therapeutic approaches.Frontiers in endocrinology · 2025Review
- Direct and indirect regulation of bone metabolism by lactoferrin.Frontiers in endocrinology · 2025Review
- Visomitin Attenuates Pathological Bone Loss by Reprogramming Osteoclast Metabolism via the STAT3/LDHB Axis.Research (Washington, D.C.) · 2025Article
- The Role of Sirtuins in Bone Repair From the Perspective of Glucose Metabolism.International journal of general medicine · 2025Review
- Nuciferine inhibits osteoclast formation through suppressing glycolysis metabolic programming and ROS production.The Kaohsiung journal of medical sciences · 2024Article
- Article
- Metabolic reprogramming in skeletal cell differentiation.Bone research · 2024Review
- PRMT6 Epigenetically Drives Metabolic Switch from Fatty Acid Oxidation toward Glycolysis and Promotes Osteoclast Differentiation During Osteoporosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Bone metabolism - an underappreciated player.npj metabolic health and disease · 2024Review
- Unraveling the intricacies of osteoclast differentiation and maturation: insight into novel therapeutic strategies for bone-destructive diseases.Experimental & molecular medicine · 2024Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Osteoclasts seem to be metabolic active during their differentiation and bone-resorptive activation. However, the functional role of lactate dehydrogenase (LDH), a tetrameric enzyme consisting of an A and/or B subunit that catalyzes interconversion of pyruvate to lactate, in RANKL-induced osteoclast differentiation is not known. In this study, RANKL treatment induced gradual gene expression and activation of the LDH A2B2 isotype during osteoclast differentiation as well as the LDH A1B3 and B4 isotypes during osteoclast maturation after pre-osteoclast formation. Glucose consumption and lactate production in growth media were accelerated during osteoclast differentiation, together with enhanced expression of H+-lactate co-transporter and increased extracellular acidification, demonstrating that glycolytic metabolism was stimulated during differentiation. Further, oxygen consumption via mitochondria was stimulated during osteoclast differentiation. On the contrary, depletion of LDH-A or LDH-B subunit suppressed both glycolytic and mitochondrial metabolism, resulting in reduced mature osteoclast formation via decreased osteoclast precursor fusion and down-regulation of the osteoclastogenic critical transcription factor NFATc1 and its target genes. Collectively, our findings suggest that RANKL-induced LDH activation stimulates glycolytic and mitochondrial respiratory metabolism, facilitating mature osteoclast formation via osteoclast precursor fusion and NFATc1 signaling.
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Registered trials
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