ArticleEndocrine2024
The unique role of bone marrow adipose tissue in ovariectomy-induced bone loss in mice.
Article in Endocrine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 15 citations in OpenAlex.
- Estrogen deficiency as a common driver and integrative mechanism in osteoporosis‑osteoarthritis comorbidity (Review).Molecular medicine reports · 2026Review
- Disuse Bone Loss After Spinal Cord Injury: Scope and Challenges, Potential Mechanisms, Treatment, and Future Directions.Journal of the Endocrine Society · 2026Review
- Aging-related metabolic dysregulation in osteoporosis: mechanisms and therapeutic strategies.Frontiers in aging · 2026Review
- Oxidative stress and bone marrow adipocytes: Molecular mechanisms and possible implications.Journal of orthopaedic translation · 2026Review
- Research progress on the mechanisms by which gut microbiota dysbiosis remodels the bone marrow neuroimmune microenvironment to drive age-related osteoporosis.Frontiers in immunology · 2026Review
- Sterol Metabolism in Ovariectomized Rats: Potential Roles of Campesterol and 4β-Hydroxycholesterol in Osteoporosis.Lipids · 2026Article
- Article
- Bone Marrow Adipocytes as Novel Regulators of Metabolic Homeostasis: Clinical Consequences of Bone Marrow Adiposity.Current obesity reports · 2025Review
- Scorpion-Centipede extracts mitigate ovariectomy-induced osteoporosis in mice through facilitating Cx3cr1 expression.Frontiers in pharmacology · 2025Article
- Bone marrow adipocytes: key players in vascular niches, aging, and disease.Frontiers in cell and developmental biology · 2025Review
- Interplay between bone marrow adiposity and bone resorption in RANKL-mediated modelled osteoporosis.Journal of cellular physiology · 2024Article
- Function and Regulation of Bone Marrow Adipose Tissue in Health and Disease: State of the Field and Clinical Considerations.Comprehensive Physiology · 2024Review
- Role of oxytocin in bone.Frontiers in endocrinology · 2024Review
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
backgroundAccumulation of bone marrow adipose tissue (BMAT) is always seen in osteoporosis induced by estrogen deficiency. Herein, we aimed to investigate the mechanisms and consequences of this phenomenon by establishing a mouse model of osteoporosis caused by ovariectomy (OVX)-mimicked estrogen deficiency.
methodsMicro-CT, osmium tetroxide staining, and histological analyses were performed to examine the changes in bone microstructure, BMAT and white adipose tissue (WAT) in OVX mice compared to sham mice. The osteogenesis and adipogenesis of primary bone marrow stromal cells (BMSCs) isolated from sham and OVX mice were compared in vitro. The molecular phenotypes of BMAT and WAT were determined and compared by quantitative PCR (qPCR). Bone marrow adipocyte-conditioned medium (BMA CM) was prepared from sham or OVX mice for coculture assays, and BMSCs or bone marrow monocytes/macrophages (BMMs) were isolated and subjected to osteoblast and osteoclast differentiation, respectively. Cell staining and qPCR were used to assess the effects of BMAT on bone metabolism.
resultsOVX-induced estrogen deficiency induced reductions in both cortical and trabecular bone mass along with an expansion of BMAT volume. At the cellular level, loss of estrogen inhibited BMSC osteogenesis and promoted BMSC adipogenesis, whereas addition of estradiol exerted the opposite effects. In response to estrogen deficiency, despite the common proinflammatory molecular phenotype observed in both fat depots, BMAT, unlike WAT, unexpectedly exhibited an increase in adipocyte differentiation and lipolytic activity as well as the maintenance of insulin sensitivity. Importantly, BMAT, but not WAT, presented increased mRNA levels of both BMP receptor inhibitors (Grem1, Chrdl1) and Rankl following OVX. In addition, treatment with BMA CM, especially from OVX mice, suppressed the osteoblast differentiation of BMSCs while favoring the osteoclast differentiation of BMMs.
conclusionOur study illustrates that OVX-induced estrogen deficiency results in bone loss and BMAT expansion by triggering imbalance between the osteogenesis and adipogenesis of BMSCs. Furthermore, expanded BMAT, unlike typical WAT, may negatively regulate bone homeostasis through paracrine inhibition of osteoblast-mediated bone formation and promotion of osteoclast-mediated bone resorption.
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