ArticleMolecular metabolism2015
Genetic determination of the cellular basis of the ghrelin-dependent bone remodeling.
Article in Molecular metabolism, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 15 citations in OpenAlex.
- Current insights into circulating biomarkers and their potential for predicting adolescent idiopathic scoliosis progression.Frontiers in cell and developmental biology · 2026Review
- Three-dimensional visualization of neural networks inside bone by Osteo-DISCO protocol and alteration of bone remodeling by surgical nerve ablation.Scientific reports · 2023Article
- Ghrelin uses the GHS-R1a/Gi/cAMP pathway and induces differentiation only in mature osteoblasts. This ghrelin pathway is impaired in AIS patients.Biochemistry and biophysics reports · 2020Article
- The role of GPCRs in bone diseases and dysfunctions.Bone research · 2019Review
- High Ghrelin Level Predicts the Curve Progression of Adolescent Idiopathic Scoliosis Girls.BioMed research international · 2018Article
- Adipokines in bone disease.Nature reviews. Rheumatology · 2016Review
- Prevention of Bone Loss in a Model of Postmenopausal Osteoporosis through Adrenomedullin Inhibition.Frontiers in physiology · 2016Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
objectiveBone mass is maintained through a balance of bone formation and resorption. This homeostatic balance is regulated by various systems involving humoral and local factors. The discovery that the anorexigenic hormone leptin regulates bone mass via neuronal pathways revealed that neurons and neuropeptides are intimately involved in bone homeostasis. Ghrelin is a stomach-derived orexigenic hormone that counteracts leptin's action. However, the physiological role of ghrelin in bone homeostasis remains unknown. In this study, through the global knockout of ghrelin receptor (Ghsr) followed by tissue-specific re-expression, we addressed the molecular basis of the action of ghrelin in bone remodeling in vivo.
methodsWe performed molecular, genetic and cell biological analyses of Ghsr-null mice and Ghsr-null mice with tissue specific Ghsr restoration. Furthermore, we evaluated the molecular mechanism of ghrelin by molecular and cell-based assays.
resultsGhsr-null mice showed a low bone mass phenotype with poor bone formation. Restoring the expression of Ghsr specifically in osteoblasts, and not in osteoclasts or the central nervous system, ameliorated bone abnormalities in Ghsr-null mice. Cell-based assays revealed ghrelin induced the phosphorylation of CREB and the expression of Runx2, which in turn accelerated osteoblast differentiation.
conclusionsOur data show that ghrelin regulates bone remodeling through Ghsr in osteoblasts by modulating the CREB and Runx2 pathways.
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