ArticleeLife2021
Adipsin promotes bone marrow adiposity by priming mesenchymal stem cells.
Article in eLife, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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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
50 citing papers in PubMed, 66 citations in OpenAlex.
- Why Do We Lose Bone During Weight Loss: Can It Be Prevented?Current osteoporosis reports · 2026Review
- Glucose-dependent regulation of hepatic adipsin controls glucose uptake and tolerance.Molecular medicine (Cambridge, Mass.) · 2026Article
- Bone as an endocrine regulator of lipid and energy metabolism.Reviews in endocrine & metabolic disorders · 2026Review
- Targeting adipocyte ESRRA alleviates osteoarthritis via interrupting inter-organelle crosstalk of complement C3-CFD-MAC cascade.Bone research · 2026Article
- Bone Marrow Immunometabolic Remodeling in Osteoporosis: From Systemic Risk Factors to Precision Intervention.International journal of general medicine · 2026Review
- Angiopoietin-like 8 governs osteoblast-adipocyte lineage commitment during skeletal aging.JCI insight · 2025Article
- Weight loss induced bone loss: mechanism of action and clinical implications.Bone research · 2025Review
- Experimental analysis of bone marrow adipose tissue and bone marrow adipocytes: An update from the bone marrow adiposity society (BMAS).Bone reports · 2025Review
- In vivo self-renewal and expansion of quiescent stem cells from a non-human primate.Nature communications · 2025Article
- Therapeutic potential of total flavonoids of Rhizoma Drynariae: inhibiting adipogenesis and promoting osteogenesis via MAPK/HIF-1α pathway in primary osteoporosis.Journal of orthopaedic surgery and research · 2025Article
- Article
- Progress in understanding how clock genes regulate aging and associated metabolic processes.Frontiers in physiology · 2025Review
- Altered metabolomics and inflammatory transcriptomics in human bone marrow adipocytes after acute high calorie diet and acute fasting.Frontiers in endocrinology · 2025Article
- Adiposity and Mineral Balance in Chronic Kidney Disease.Current osteoporosis reports · 2024Review
- In nondiabetic C57BL/6J mice, canagliflozin affects the skeleton in a sex- and age-dependent manner.JBMR plus · 2024Article
- Decoding senescence of aging single cells at the nexus of biomaterials, microfluidics, and spatial omics.npj aging · 2024Review
- Serum Leucine-Rich Alpha-2 Glycoprotein 1 Levels in Patients with Lipodystrophy Syndromes.Biomolecules · 2024Article
- Calorie restriction in mice impairs cortical but not trabecular peak bone mass by suppressing bone remodeling.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2024Article
- Adipsin-dependent adipocyte maturation induces cancer cell invasion in breast cancer.Scientific reports · 2024Article
- Pathology of Diabetes-Induced Immune Dysfunction.International journal of molecular sciences · 2024Review
Corrections and comments
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Authors and funding
20 authors at 7 institutions in 2 countries.
Funding
Abstract
Background: Marrow adipose tissue (MAT) has been shown to be vital for regulating metabolism and maintaining skeletal homeostasis in the bone marrow (BM) niche. As a reflection of BM remodeling, MAT is highly responsive to nutrient fluctuations, hormonal changes, and metabolic disturbances such as obesity and diabetes mellitus. Expansion of MAT has also been strongly associated with bone loss in mice and humans. However, the regulation of BM plasticity remains poorly understood, as does the mechanism that links changes in marrow adiposity with bone remodeling. Methods: We studied deletion of Adipsin, and its downstream effector, C3, in C57BL/6 mice as well as the bone-protected PPARγ constitutive deacetylation 2KR mice to assess BM plasticity. The mice were challenged with thiazolidinedione treatment, calorie restriction, or aging to induce bone loss and MAT expansion. Analysis of bone mineral density and marrow adiposity was performed using a μCT scanner and by RNA analysis to assess adipocyte and osteoblast markers. For Results: We show that Adipsin is the most upregulated adipokine during MAT expansion in mice and humans in a PPARγ acetylation-dependent manner. Genetic ablation of Adipsin in mice specifically inhibited MAT expansion but not peripheral adipose depots, and improved bone mass during calorie restriction, thiazolidinedione treatment, and aging. These effects were mediated through its downstream effector, complement component C3, to prime common progenitor cells toward adipogenesis rather than osteoblastogenesis through inhibiting Wnt/β-catenin signaling. Conclusions: Adipsin promotes new adipocyte formation and affects skeletal remodeling in the BM niche. Our study reveals a novel mechanism whereby the BM sustains its own plasticity through paracrine and endocrine actions of a unique adipokine. Funding: This work was supported by the National Institutes of Health T32DK007328 (NA), F31DK124926 (NA), R01DK121140 (JCL), R01AR068970 (BZ), R01AR071463 (BZ), R01DK112943 (LQ), R24DK092759 (CJR), and P01HL087123 (LQ).
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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.