ArticleiScience2022
Partial prevention of glucocorticoid-induced osteocyte deterioration in young male mice with osteocrin gene therapy.
Article in iScience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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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.
The trial behind it
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Who cites it
8 citing papers in PubMed, 15 citations in OpenAlex.
- Genome-wide CRISPR interference screen identifies Clip2 as a novel regulator of osteocyte maturation and morphology.The Journal of biological chemistry · 2026Article
- Harmine ameliorates steroid-induced osteonecrosis of the femoral head by modulating metabolism and ferroptosis via HIF1-α.Fundamental research · 2026Article
- The pivotal role of the Hes1/Piezo1 pathway in the pathophysiology of glucocorticoid-induced osteoporosis.JCI insight · 2024Article
- Crosstalk between bone and brain in Alzheimer's disease: Mechanisms, applications, and perspectives.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024Review
- The osteocytic actions of glucocorticoids on bone mass, mechanical properties, or perilacunar remodeling outcomes are not rescued by PTH(1-34).Frontiers in endocrinology · 2024Article
- Exogenous melatonin ameliorates steroid-induced osteonecrosis of the femoral head by modulating ferroptosis through GDF15-mediated signaling.Stem cell research & therapy · 2023Article
- Pathogenic mechanisms of glucocorticoid-induced osteoporosis.Cytokine & growth factor reviews · 2023Review
- SP7: from Bone Development to Skeletal Disease.Current osteoporosis reports · 2023Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
Glucocorticoid excess suppresses osteocyte remodeling of surrounding bone minerals, causes apoptosis of osteoblasts and osteocytes, and disrupts bone remodeling, eventually, leading to glucocorticoid-induced osteoporosis and bone fragility. Preventing apoptosis and preserving osteocyte morphology could be an effective means of preventing bone loss during glucocorticoid treatment. We hypothesized that osteocrin, which preserves osteocyte viability and morphology in Sp7-deficient mice, could prevent osteocyte death and dysfunction in a glucocorticoid excess model. We used adeno-associated virus (AAV8) to induce osteocrin overexpression in mice one week before implantation with prednisolone or placebo pellets. After 28 days, prednisolone caused the expected reduction in cortical bone thickness and osteocyte canalicular length in control AAV8-treated mice, and these effects were blunted in mice receiving AAV8-osteocrin. Glucocorticoid-induced changes in cortical porosity, trabecular bone mass, and gene expression were not prevented by osteocrin. These findings support a modest therapeutic potential for AAV8-osteocrin in preserving osteocyte morphology during disease.
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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.