ArticleThe Journal of biological chemistry2013
Genetic deletion of catalytic subunits of AMP-activated protein kinase increases osteoclasts and reduces bone mass in young adult mice.
Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 59 citations in OpenAlex.
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- Trelagliptin stimulates osteoblastic differentiation by increasing runt-related transcription factor 2 (RUNX2): a therapeutic implication in osteoporosis.Bioengineered · 2021Article
- Induction of osteoclast formation by LOX mutant (LOXG473A) through regulation of autophagy.Annals of translational medicine · 2021Article
- Transcriptomics-based analysis of the mechanism by which Wang-Bi capsule alleviates joint destruction in rats with collagen-induced arthritis.Chinese medicine · 2021Article
- Maternal Inactivity Programs Skeletal Muscle Dysfunction in Offspring Mice by Attenuating Apelin Signaling and Mitochondrial Biogenesis.Cell reports · 2020Article
- Suppression of AMP-activated protein kinase reverses osteoprotegerin-induced inhibition of osteoclast differentiation by reducing autophagy.Cell proliferation · 2020Article
- Role of Altered Metabolic Microenvironment in Osteolytic Metastasis.Frontiers in cell and developmental biology · 2020Review
- AMPK: implications in osteoarthritis and therapeutic targets.American journal of translational research · 2020Review
- Extracellular vesicles in bone: "dogrobbers" in the "eternal battle field".Cell communication and signaling : CCS · 2019Review
- Dose-dependent roles of aspirin and other non-steroidal anti-inflammatory drugs in abnormal bone remodeling and skeletal regeneration.Cell & bioscience · 2019Review
- Role of Metformin on Osteoblast Differentiation in Type 2 Diabetes.BioMed research international · 2019Review
- Metformin suppresses UHMWPE particle-induced osteolysis in the mouse calvaria by promoting polarization of macrophages to an anti-inflammatory phenotype.Molecular medicine (Cambridge, Mass.) · 2018Article
Corrections and comments
- Erratum issued
Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
AMP-activated protein kinase (AMPK) is a key regulator of cellular and systemic energy homeostasis and a potential therapeutic target for the intervention of cancer and metabolic disorders. However, the role of AMPK in bone homeostasis remains incompletely understood. Here we assessed the skeletal phenotype of mice lacking catalytic subunits of AMPK and found that mice lacking AMPKα1 (Prkaa1(-/-)) or AMPKα2 (Prkaa2(-/-)) had reduced bone mass compared with the WT mice, although the reduction was less in Prkaa2(-/-) mice than in Prkaa1(-/-) mice. Static and dynamic bone histomorphometric analyses revealed that Prkaa1(-/-) mice had an elevated rate of bone remodeling because of increases in bone formation and resorption, whereas AMPKα2 KO-induced bone mass reduction was largely attributable to elevated bone resorption. In agreement with our in vivo results, AMPKα deficiency was associated with increased osteoclastogenesis in vitro. Moreover, we found that AMPKα1 inhibited the receptor activator of nuclear factor κB (RANK) signaling, providing an explanation for AMPK-mediated inhibition of osteoclastogenesis. Therefore, our findings further underscore the importance of AMPK in bone homeostasis, in particular osteoclastogenesis, in young adult mammals.
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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.