ArticleThe Journal of clinical investigation2024
Excess glucocorticoids inhibit murine bone turnover via modulating the immunometabolism of the skeletal microenvironment.
Article in The Journal of clinical investigation, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.
What it found
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
28 citing papers in PubMed, 1 synthesis or guideline pooled it, 24 citations in OpenAlex.
- The role of CD8Frontiers in immunology · 2026Pooled it
- Low-dose oral nicotinamide mononucleotide for immune thrombocytopenia: a phase 1/2 trial.Nature medicine · 2026Trial
- ADSC-derived mitochondrial nanovesicles transplantation alleviates capsular fibrosis and inflammation and improves joint mobility in a rat model of adhesive capsulitis.Journal of orthopaedic translation · 2026Article
- 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
- Tri-modal nanocatalytic microenvironment regulations for macrophage reprogramming and osteoporotic fracture healing promotion.Materials today. Bio · 2026Article
- FTMT-mediated suppression of mitophagy links iron accumulation to osteoporosis.Redox biology · 2026Article
- Immunometabolism of macrophages in the bone microenvironment: a new perspective for bone healing therapy.Journal of advanced research · 2026Review
- Adipose-Derived Stem Cell Membrane-Coated Mitochondria Restore Tendon Stromal Cell Function Through Metabolic Reprogramming and Promote Achilles Tendon Healing.Journal of functional biomaterials · 2026Article
- Advances in the mechanism for steroid-induced osteonecrosis of the femoral head.Bone research · 2026Review
- Sulfated chitosan mitigates acute lung injury induced bone loss via immunoregulation.Bone research · 2026Article
- Bone health in asthma: a twofold effect of disease and pharmacotherapy.Frontiers in endocrinology · 2026Review
- Interorgan Communications in Skeletal Pathophysiology: From Molecular Pathways to Multidisciplinary Therapies.Research (Washington, D.C.) · 2026Review
- Multiscale bone remodeling in COVID-19: from osteoimmune signaling to structural and mechanical impairment.Frontiers in bioengineering and biotechnology · 2026Review
- Bone and muscle crosstalk in steroid-induced osteonecrosis of the femoral head: a four-axis pathophysiological framework.Frontiers in immunology · 2026Review
- Efficacy and immune-inflammatory modulation of combined glucocorticoid and anti-tuberculosis therapy in patients with bronchial asthma and pulmonary tuberculosis.American journal of translational research · 2026Article
- Up-regulation of Ifi27l2a expression in bone marrow monocytes contributes to glucocorticoid-induced bone loss.Communications biology · 2025Article
- Unraveling Ginsenoside Rg1's osteoprotective pathways in zebrafish models of glucocorticoid induced osteoporosis via transcriptomics.Scientific reports · 2025Article
- Basigin links altered skeletal stem cell lineage dynamics with glucocorticoid-induced bone loss and impaired angiogenesis.Nature communications · 2025Article
- Progress of research on the gut microbiome and its metabolite short-chain fatty acids in postmenopausal osteoporosis: a literature review.Frontiers of medicine · 2025Review
- Targeted Delivery of α-ketoglutarate to Macrophages in Bone: A Novel Therapeutic Strategy for Improving Fracture Healing in Type 2 Diabetes.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
Corrections and comments
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Authors and funding
20 authors at 3 institutions in 5 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Elevated bone resorption and diminished bone formation have been recognized as the primary features of glucocorticoid-associated skeletal disorders. However, the direct effects of excess glucocorticoids on bone turnover remain unclear. Here, we explored the outcomes of exogenous glucocorticoid treatment on bone loss and delayed fracture healing in mice and found that reduced bone turnover was a dominant feature, resulting in a net loss of bone mass. The primary effect of glucocorticoids on osteogenic differentiation was not inhibitory; instead, they cooperated with macrophages to facilitate osteogenesis. Impaired local nutrient status - notably, obstructed fatty acid transportation - was a key factor contributing to glucocorticoid-induced impairment of bone turnover in vivo. Furthermore, fatty acid oxidation in macrophages fueled the ability of glucocorticoid-liganded receptors to enter the nucleus and then promoted the expression of BMP2, a key cytokine that facilitates osteogenesis. Metabolic reprogramming by localized fatty acid delivery partly rescued glucocorticoid-induced pathology by restoring a healthier immune-metabolic milieu. These data provide insights into the multifactorial metabolic mechanisms by which glucocorticoids generate skeletal disorders, thus suggesting possible therapeutic avenues.
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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 Socratic graph.