ArticleBritish journal of pharmacology2020
The low-expression programming of 11β-HSD2 mediates osteoporosis susceptibility induced by prenatal caffeine exposure in male offspring rats.
Article in British journal of pharmacology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 36 citations in OpenAlex.
- The histone deacetylase family in health and disease.Signal transduction and targeted therapy · 2026Review
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- Molecular mechanisms and translational prospects in osteoporosis.Frontiers in endocrinology · 2026Review
- Pregnancy and Caffeine Metabolism: Updated Insights and Implications for Maternal-Fetal Health.Nutrients · 2025Review
- Article
- Review
- Metabolic Rewiring and Post-Translational Modifications: Unlocking the Mechanisms of Bone Turnover in Osteoporosis.Aging and disease · 2025Review
- Article
- Dexamethasone exposure during pregnancy triggers metabolic syndrome in offspring via epigenetic alteration of IGF1.Cell communication and signaling : CCS · 2024Article
- Prenatal glucocorticoids exposure and adverse cardiovascular effects in offspring.Frontiers in endocrinology · 2024Review
- The Epigenetic Effects of Coffee.Molecules (Basel, Switzerland) · 2023Review
- Therapeutic approach of natural products that treat osteoporosis by targeting epigenetic modulation.Frontiers in genetics · 2023Review
- BMSC-derived exosomes promote tendon-bone healing after anterior cruciate ligament reconstruction by regulating M1/M2 macrophage polarization in rats.Stem cell research & therapy · 2022Article
- HDAC11, an emerging therapeutic target for metabolic disorders.Frontiers in endocrinology · 2022Review
- Role of histone modification in the occurrence and development of osteoporosis.Frontiers in endocrinology · 2022Review
- The low-expression programming of 11β-HSD2 mediates osteoporosis susceptibility induced by prenatal caffeine exposure in male offspring rats.British journal of pharmacology · 2020Article
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
background and purposePrenatal caffeine exposure (PCE) can cause developmental toxicity of long bones in offspring, but the long-term effects and the underlying mechanism have not been fully clarified. Here, we investigated the effects of PCE peak bone mass accumulation and osteoporosis susceptibility in offspring and its intrauterine programming mechanism. EXPERIMENTAL APPROACH: Pregnant Wistar rats were administrated intragastrically with saline or caffeine (120 mg·kg KEY
resultsPCE caused fetal bone dysplasia in male and female offspring. In adulthood, PCE reduced peak bone mass and increased osteoporosis susceptibility in male offspring but not in females. Meanwhile, PCE only decreased the H3K9ac and expression levels of 11β-hydroxysteroid dehydrogenase 2 (11β-HSD2) before and after birth in the male offspring but not in the females. Moreover, the high level of corticosterone induced by PCE down-regulated the H3K9ac and expression levels of 11β-HSD2 through promoting glucocorticoid receptor (GR; NR3C1) into the nucleus of bone marrow mesenchymal stem cells (BMSCs) and recruiting histone deacetylase 11 (HDAC11) binding to 11β-HSD2 promoter region, which further enhanced the effect of corticosterone on suppressing osteogenic function of BMSCs. CONCLUSION AND IMPLICATIONS: PCE caused osteoporosis susceptibility in male adult offspring, which attributed to the low-functional programming of 11β-HSD2 induced by corticosterone via GR/HDAC11 signalling.
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