ArticleScientific reports2016
Mesenchymal progenitors in osteopenias of diverse pathologies: differential characteristics in the common shift from osteoblastogenesis to adipogenesis.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed.
- Targeting the osteoporotic bone microenvironment: Mechanistic insight and therapeutic biomaterials for accelerating bone regeneration.Bioactive materials · 2026Review
- The role and mechanisms of bone microenvironment regulators in osteoporosis: novel intervention strategies for addressing the challenges of aging.Frontiers in endocrinology · 2026Review
- Therapeutic Management of Glucocorticoid-Induced Osteoporosis with a Focus on Older Adults: A Narrative Review.Drugs & aging · 2026Review
- A novel strategy for bone defect repair: Stromal cell-derived factor 1α sustained-release acellular fish scale scaffolds combined with injection of bone marrow mesenchymal stem cells promote bone regeneration.Materials today. Bio · 2025Article
- YAP1 mediates the dimensional and chemical coordination of immunoregulation and therapy in extensively passaged mesenchymal stem cells.Theranostics · 2025Article
- Integrated Phenotypic and Transcriptomic Analyses of Osteoporosis in Type 2 Diabetic Mice.International journal of medical sciences · 2025Article
- Single-cell multi-omics identify novel regulators required for osteoclastogenesis during aging.iScience · 2024Article
- Osteoporosis under psychological stress: mechanisms and therapeutics.Life medicine · 2024Review
- NOX4-reactive oxygen species axis: critical regulators of bone health and metabolism.Frontiers in cell and developmental biology · 2024Review
- The assessment of marrow adiposity in type 1 diabetic rabbits through magnetic resonance spectroscopy is linked to bone resorption.Frontiers in endocrinology · 2024Article
- MiR-601-induced BMSCs senescence accelerates steroid-induced osteonecrosis of the femoral head progression by targeting SIRT1.Cellular and molecular life sciences : CMLS · 2023Article
- Inhibition of C5AR1 impairs osteoclast mobilization and prevents bone loss.Molecular therapy : the journal of the American Society of Gene Therapy · 2023Article
- Review
- Residual periodontal ligament in the extraction socket promotes the dentin regeneration potential of DPSCs in the rabbit jaw.Stem cell research & therapy · 2023Article
- Update on the Role of Glucocorticoid Signaling in Osteoblasts and Bone Marrow Adipocytes During Aging.Current osteoporosis reports · 2023Review
- Mesenchymal stem cells: Emerging concepts and recent advances in their roles in organismal homeostasis and therapy.Frontiers in cellular and infection microbiology · 2023Review
- Eldecalcitol prevented OVX-induced osteoporosis through inhibiting BMSCs senescence by regulating the SIRT1-Nrf2 signal.Frontiers in pharmacology · 2023Article
- Melatonin suppresses bone marrow adiposity in ovariectomized rats by rescuing the imbalance between osteogenesis and adipogenesis through SIRT1 activation.Journal of orthopaedic translation · 2023Article
- Extracellular vesicles derived from neural EGFL-Like 1-modified mesenchymal stem cells improve acellular bone regeneration via the miR-25-5p-SMAD2 signaling axis.Bioactive materials · 2022Article
- Tocotrienol as a Protecting Agent against Glucocorticoid-Induced Osteoporosis: A Mini Review of Potential Mechanisms.Molecules (Basel, Switzerland) · 2022Review
Corrections and comments
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Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Osteoporosis is caused by pathologic factors such as aging, hormone deficiency or excess, inflammation, and systemic diseases like diabetes. Bone marrow stromal cells (BMSCs), the mesenchymal progenitors for both osteoblasts and adipocytes, are modulated by niche signals. In differential pathologic states, the pathological characteristics of BMSCs to osteoporoses and functional differences are unknown. Here, we detected that trabecular bone loss co-existed with increased marrow adiposity in 6 osteoporotic models, respectively induced by natural aging, accelerated senescence (SAMP6), ovariectomy (OVX), type 1 diabetes (T1D), excessive glucocorticoids (GIOP) and orchidectomy (ORX). Of the ex vivo characteristics of BMSCs, the colony-forming efficiency and the proliferation rate in aging, SAMP6, OVX, GIOP and ORX models decreased. The apoptosis and cellular senescence increased except in T1D, with up-regulation of p53 and p16 expression. The osteogenesis declined except in GIOP, with corresponding down-regulation of Runt-related transcription factor 2 (RUNX2) expression. The adipogenesis increased in 6 osteoporotic models, with corresponding up-regulation of Peroxisome proliferator activated receptor gamma (PPARγ) expression. These findings revealed differential characteristics of BMSCs in a common shift from osteoblastogenesis to adipogenesis among different osteoporoses and between sexes, and provide theoretical basis for the functional modulation of resident BMSCs in the regenerative therapy for osteoporosis.
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