ArticleJCI insight2022
Constitutive bone marrow adipocytes suppress local bone formation.
Article in JCI insight, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.
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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.
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Who cites it
42 citing papers in PubMed, 1 synthesis or guideline pooled it, 62 citations in OpenAlex.
- Deep learning and genome-wide association meta-analyses of bone marrow adiposity in the UK Biobank.Nature communications · 2025Pooled it
- Not just fillers: the emerging role of bone marrow adipocytes in bone and bone marrow homeostasis.Biology open · 2026Review
- Transcriptomic analysis of bone marrow adipose tissue reveals enrichment in lipid transport in response to a Western diet.Endocrinology · 2026Article
- Recent advances in glucocorticoid regulation of bone and the bone marrow niche: Genetic and pharmacological approaches to understand and prevent bone loss.Current opinion in endocrine and metabolic research · 2026Article
- Youthfulness of marrow AdipoqBone research · 2026Article
- Article
- Exosome-derived LncRNAs in bone remodeling: recent advances and future directions for bone disease therapy.Stem cell research & therapy · 2026Review
- Expansion of bone marrow adipocytes in obese mice leads to PD-L1-driven bone marrow immunosuppression and osteoclastogenesis.Bone research · 2026Article
- Fostering the next generation of bone marrow adiposity researchers: the 3rd International Bone Marrow Adiposity Society Summer School 2025 report.Biology open · 2026Article
- Advances in Adipose Tissue Biology.Endocrine reviews · 2026Review
- A catecholamine-independent pathway controlling adaptive adipocyte lipolysis.Nature metabolism · 2026Article
- Bone marrow adipoq-lineage cells in regulating the bone and marrow microenvironment: identities, functions, and mechanisms.Frontiers in endocrinology · 2026Review
- Bifurcate Regulation of Hematopoietic Homeostasis and Bone Osteogenesis by VHL-HIF2α-Controlled Adipocyte Function.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- The protective role of adipogenic lineage precursors in maintaining bone marrow redox homeostasis in a mouse model of prenatal dexamethasone exposure.Redox biology · 2025Article
- Experimental analysis of bone marrow adipose tissue and bone marrow adipocytes: An update from the bone marrow adiposity society (BMAS).Bone reports · 2025Review
- Effects of FGF21, soluble TGFBR2, and environmental temperature on metabolic dysfunction in lipodystrophic mice.JCI insight · 2025Article
- Depletion of marrow adipo-CAR cells in mice enhances bone formation by activating bone morphogenetic protein receptor (BMPR) in pre-osteoblasts.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2025Article
- Association of the Chinese visceral adiposity index with marrow adiposity in postmenopausal females.Frontiers in endocrinology · 2025Article
- Autophagy: regulating the seesaw of bone-fat balance.Frontiers in cell and developmental biology · 2025Review
- Foxk2 Enhances Adipogenic Differentiation by Relying on the Transcriptional Activation of Peroxisome Proliferator-Activated Receptor Gamma.Journal of cellular and molecular medicine · 2025Article
Corrections and comments
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Authors and funding
15 authors at 2 institutions in 2 countries.
Funding
Abstract
BM adipocytes (BMAd) are a unique cell population derived from BM mesenchymal progenitors and marrow adipogenic lineage precursors. Although they have long been considered to be a space filler within bone cavities, recent studies have revealed important physiological roles in hematopoiesis and bone metabolism. To date, the approaches used to study BMAd function have been confounded by contributions by nonmarrow adipocytes or by BM stromal cells. To address this gap in the field, we have developed a BMAd-specific Cre mouse model to deplete BMAds by expression of diphtheria toxin A (DTA) or by deletion of peroxisome proliferator-activated receptor gamma (Pparg). We found that DTA-induced loss of BMAds results in decreased hematopoietic stem and progenitor cell numbers and increased bone mass in BMAd-enriched locations, including the distal tibiae and caudal vertebrae. Elevated bone mass appears to be secondary to enhanced endosteal bone formation, suggesting a local effect caused by depletion of BMAd. Augmented bone formation with BMAd depletion protects mice from bone loss induced by caloric restriction or ovariectomy, and it facilitates the bone-healing process after fracture. Finally, ablation of Pparg also reduces BMAd numbers and largely recapitulates high-bone mass phenotypes observed with DTA-induced BMAd depletion.
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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.