ArticleWorld journal of stem cells2021
Transcriptomic alterations underline aging of osteogenic bone marrow stromal cells.
Article in World journal of stem cells, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 3 citations in OpenAlex.
- GDF11 activates AMPK-dependent mitophagy to drive osteogenic differentiation of rat bone marrow mesenchymal stem cells.American journal of stem cells · 2026Article
- Senescence of bone marrow mesenchymal stromal cells: a narrative review of mechanisms, functional consequences, and rejuvenation strategies for age-related disorders.Stem cell research & therapy · 2025Review
- Pathological and Inflammatory Consequences of Aging.Biomolecules · 2025Review
- TP53-mediated miR-2861 promotes osteogenic differentiation of BMSCs by targeting Smad7.Molecular and cellular biochemistry · 2022Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMultipotent bone marrow stromal cells (BMSCs) are adult stem cells that form functional osteoblasts and play a critical role in bone remodeling. During aging, an increase in bone loss and reduction in structural integrity lead to osteoporosis and result in an increased risk of fracture. We examined age-dependent histological changes in murine vertebrae and uncovered that bone loss begins as early as the age of 1 mo.
aimTo identify the functional alterations and transcriptomic dynamics of BMSCs during early bone loss.
methodsWe collected BMSCs from mice at early to middle ages and compared their self-renewal and differentiation potential. Subsequently, we obtained the transcriptomic profiles of BMSCs at 1 mo, 3 mo, and 7 mo.
resultsThe colony-forming and osteogenic commitment capacity showed a comparable finding that decreased at the age of 1 mo. The transcriptomic analysis showed the enrichment of osteoblastic regulation genes at 1 mo and loss of osteogenic features at 3 mo. The BMSCs at 7 mo showed enrichment of adipogenic and DNA repair features. Moreover, we demonstrated that the WNT and MAPK signaling pathways were upregulated at 1 mo, followed by increased pro-inflammatory and apoptotic features.
conclusionOur study uncovered the cellular and molecular dynamics of bone aging in mice and demonstrated the contribution of BMSCs to the early stage of age-related bone loss.
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