ArticleCurrent opinion in endocrine and metabolic research2026
Recent advances in glucocorticoid regulation of bone and the bone marrow niche: Genetic and pharmacological approaches to understand and prevent bone loss.
Article in Current opinion in endocrine and metabolic research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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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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Abstract
Glucocorticoids are essential steroid hormones whose excess - whether from therapeutic use or endogenous overproduction - causes significant bone loss and fracture risk. In bone, glucocorticoids act directly on osteoblasts, osteocytes, and osteoclasts via the glucocorticoid receptor and indirectly through bone marrow adipose tissue and shared mesenchymal progenitors. An important mechanism involves suppression of canonical Wnt/β-catenin signaling, which reduces osteogenesis and increases marrow adiposity. Several pharmacological and plant-derived compounds with therapeutic promise target Wnt and other glucocorticoid-regulated signaling pathways. Emerging evidence highlights intermediary and potential therapeutic roles for niche-derived extracellular vesicles in bone loss associated with glucocorticoids. Comparing results between studies is complicated by underreporting of environmental and biological variables that may interact with glucocorticoids to affect bone or the marrow niche, which underscores the need for greater methodological rigor in preclinical studies.
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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.