ArticleAging cell2020
Increased marrow adipogenesis does not contribute to age-dependent appendicular bone loss in female mice.
Article in Aging cell, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
What it found
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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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
29 citing papers in PubMed, 34 citations in OpenAlex.
- Transcriptomic analysis of bone marrow adipose tissue reveals enrichment in lipid transport in response to a Western diet.Endocrinology · 2026Article
- Article
- Cellular signaling crosstalk between osteoporosis and diabetes: Common mechanisms and therapeutic targets (Review).Biomedical reports · 2026Review
- Addressing osteoblast senescence: Molecular pathways and the frontier of anti-ageing treatments.Clinical and translational medicine · 2025Review
- 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
- Skeletal stem and progenitor cells in bone physiology, ageing and disease.Nature reviews. Endocrinology · 2025Review
- Bone Marrow Adipocytes as Novel Regulators of Metabolic Homeostasis: Clinical Consequences of Bone Marrow Adiposity.Current obesity reports · 2025Review
- Interplay between bone marrow adiposity and bone resorption in RANKL-mediated modelled osteoporosis.Journal of cellular physiology · 2024Article
- Long-Term Follow-up After Ovariectomy Reveals Correlations Between Bone Marrow Adiposity and Trabecular Bone Quality in the Proximal Metaphysis of Tibiae in Rats.Calcified tissue international · 2024Article
- Hdac3-deficiency increases senescence-associated distention of satellite DNA and telomere-associated foci in osteoprogenitor cells.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2024Article
- Preclinical Rodent Models for Human Bone Disease, Including a Focus on Cortical Bone.Endocrine reviews · 2024Review
- Function and Regulation of Bone Marrow Adipose Tissue in Health and Disease: State of the Field and Clinical Considerations.Comprehensive Physiology · 2024Review
- Effects of Systemic Peroxisome Proliferator-Activated Receptor Gamma Inhibition on Bone and Immune Cells in Aged Female Mice.The journals of gerontology. Series A, Biological sciences and medical sciences · 2024Article
- Review
- Article
- Peroxisome proliferator activated receptor-γ in osteoblasts controls bone formation and fat mass by regulating sclerostin expression.iScience · 2023Article
- Single-Cell RNA-Sequencing Reveals the Skeletal Cellular Dynamics in Bone Repair and Osteoporosis.International journal of molecular sciences · 2023Review
- Turning the spotlight on bone marrow adipocytes in haematological malignancy and non-malignant conditions.British journal of haematology · 2023Review
- Update on the Role of Glucocorticoid Signaling in Osteoblasts and Bone Marrow Adipocytes During Aging.Current osteoporosis reports · 2023Review
- Cellular dynamics of distinct skeletal cells and the development of osteosarcoma.Frontiers in endocrinology · 2023Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
Marrow adipocytes and osteoblasts differentiate from common mesenchymal progenitors in a mutually exclusive manner, and diversion of these progenitors toward adipocytes in old age has been proposed to account for the decline in osteoblasts and the development of involutional osteoporosis. This idea has been supported by evidence that thiazolidinedione (TZD)-induced activation of PPARγ, the transcription factor required for adipocyte differentiation, increases marrow fat and causes bone loss. We functionally tested this hypothesis using C57BL/6J mice with conditional deletion of PPARγ from early mesenchymal progenitors targeted by the Prx1-Cre transgene. Using a longitudinal littermate-controlled study design, we observed that PPARγ is indispensable for TZD-induced increase in marrow adipocytes in 6-month-old male mice, and age-associated increase in marrow adipocytes in 22-month-old female mice. In contrast, PPARγ is dispensable for the loss of cortical and trabecular bone caused by TZD or old age. Instead, PPARγ restrains age-dependent development of cortical porosity. These findings do not support the long-standing hypothesis that increased marrow adipocyte differentiation contributes to bone loss in old age but reveal a novel role of mesenchymal cell PPARγ in the maintenance of cortical integrity.
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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 Socratic graph.