ArticleRedox biology2025
The protective role of adipogenic lineage precursors in maintaining bone marrow redox homeostasis in a mouse model of prenatal dexamethasone exposure.
Article in Redox biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Recent advances in glucocorticoid regulation of bone and the bone marrow niche: Genetic and pharmacological approaches to understand and prevent bone loss.Current opinion in endocrine and metabolic research · 2026Article
- Bone marrow adipoq-lineage cells in regulating the bone and marrow microenvironment: identities, functions, and mechanisms.Frontiers in endocrinology · 2026Review
- Targeting type H vessels with bioactive metabolites from traditional Chinese botanical drugs: a therapeutic strategy for skeletal disorders.Frontiers in pharmacology · 2025Review
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Authors and funding
8 authors.
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Abstract
Bone marrow adipogenic precursors play important roles in bone metabolism in both young and adult mice, but their contributions to early long bone development remains poorly understood. In this study, we elucidate the role of bone marrow adipocyte lineage precursors in modulating bone marrow redox homeostasis through the secretion of fibulin-5 (Fbln5), using a prenatal dexamethasone exposure (PDE) mouse model. Our previous research demonstrates that PDE induces cellular senescence in the bone marrow, resulting in long bone growth retardation in young offspring. Extending these findings, we now reveal that PDE not only induces cellular senescence and impairs bone formation, but also disrupts type H vessels and reduces Adiponectin-expressing (Adipoq
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