ArticleThe Journal of clinical investigation2021
Bone marrow adipogenic lineage precursors promote osteoclastogenesis in bone remodeling and pathologic bone loss.
Article in The Journal of clinical investigation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 141 papers.
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Who cites it
141 citing papers in PubMed, 202 citations in OpenAlex.
- Decoding Skeletal Biology Through Transcriptomics: Insights from Bulk, Single-Cell, Spatial, and Multi-Omics Approaches.International journal of molecular sciences · 2026Review
- Skeletal stem and progenitor cell niche organization, regulation and repair.Reviews in endocrine & metabolic disorders · 2026Review
- Not just fillers: the emerging role of bone marrow adipocytes in bone and bone marrow homeostasis.Biology open · 2026Review
- Youthfulness of marrow AdipoqBone research · 2026Article
- Diets Differently Affect Bone Health: Murine Models.International journal of molecular sciences · 2026Article
- Mechanistic Links Underlying the Comorbidity of Osteoporosis and Osteoarthritis: Cell Fate Plasticity Driven by the Subchondral Bone Microenvironment.International journal of molecular sciences · 2026Review
- Intermittent parathyroid hormone employs autonomous and non-autonomous mechanisms to drive osteogenesis from Ebf3-expressing skeletal progenitor cells.bioRxiv : the preprint server for biology · 2026Article
- A RANKLBone research · 2026Article
- Metallic topological structures in bone repair implants: Design, properties, and biological interactions.Journal of orthopaedic translation · 2026Review
- Targeting the STK39/ARID2 Axis to Inhibit NF-κB Signaling: A Novel Pathway for Mesenchymal Stem Cell Osteogenic Differentiation in Osteoporosis Management.Journal of musculoskeletal & neuronal interactions · 2026Article
- Inactivation of Hes1 in Skeletal Undifferentiated Cells Increases Bone Volume.Endocrinology · 2026Article
- Estrogen signaling in PDGFRα+ cells positively regulates cortical bone metabolism via IGFBP5 in female mice.JBMR plus · 2026Article
- RANKL-convergent osteoimmune network framework in osteoporosis: integrating macrophage activation, T-cell imbalance, and cytokine crosstalk.Frontiers in immunology · 2026Review
- Oxidative stress and bone marrow adipocytes: Molecular mechanisms and possible implications.Journal of orthopaedic translation · 2026Review
- Chronic Alcohol Consumption Enhances the Differentiation Capacity of Hematopoietic Stem and Progenitor Cells into Osteoclast Precursors.The American journal of pathology · 2026Article
- Bone marrow adipoq-lineage cells in regulating the bone and marrow microenvironment: identities, functions, and mechanisms.Frontiers in endocrinology · 2026Review
- Antcin K suppresses osteoclastogenesis through modulation of the focal adhesion kinase and phosphoinositide 3-kinase pathways and attenuates ligature-induced periodontitis.Journal of dental sciences · 2026Article
- Alcohol consumption exacerbates high-fat diet-mediated disruptions in myelopoiesis and osteoclastogenesis in mouse models of metabolic dysfunction-associated liver diseases.Frontiers in endocrinology · 2026Article
- Ferritin promotes monocyte osteoclastogenic differentiation to aggravate alveolar bone resorption in periodontitis.Journal of dental sciences · 2026Article
- Chemotherapy-induced adipo-lineage cell senescence drives bone loss.Nature communications · 2025Article
81 more citing papers are in PubMed but not listed here.
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Authors and funding
16 authors at 4 institutions in 2 countries.
Funding
Abstract
Bone is maintained by coupled activities of bone-forming osteoblasts/osteocytes and bone-resorbing osteoclasts. Alterations in this relationship can lead to pathologic bone loss such as osteoporosis. It is well known that osteogenic cells support osteoclastogenesis via production of RANKL. Interestingly, our recently identified bone marrow mesenchymal cell population-marrow adipogenic lineage precursors (MALPs) that form a multidimensional cell network in bone-was computationally demonstrated to be the most interactive with monocyte-macrophage lineage cells through high and specific expression of several osteoclast regulatory factors, including RANKL. Using an adipocyte-specific Adipoq-Cre to label MALPs, we demonstrated that mice with RANKL deficiency in MALPs have a drastic increase in trabecular bone mass in long bones and vertebrae starting from 1 month of age, while their cortical bone appears normal. This phenotype was accompanied by diminished osteoclast number and attenuated bone formation at the trabecular bone surface. Reduced RANKL signaling in calvarial MALPs abolished osteolytic lesions after LPS injections. Furthermore, in ovariectomized mice, elevated bone resorption was partially attenuated by RANKL deficiency in MALPs. In summary, our studies identified MALPs as a critical player in controlling bone remodeling during normal bone metabolism and pathological bone loss in a RANKL-dependent fashion.
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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.