ArticleEndocrinology2014
An N-ethyl-N-nitrosourea induced corticotropin-releasing hormone promoter mutation provides a mouse model for endogenous glucocorticoid excess.
Article in Endocrinology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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.
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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.
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Who cites it
20 citing papers in PubMed, 30 citations in OpenAlex.
- Increased P2X7 level does not affect anxiety or stress-coping behavior in male mice.Purinergic signalling · 2026Article
- Cushing's Disease in the Animal Kingdom: Translational Insights for Human Medicine.International journal of molecular sciences · 2025Review
- Genetic models of Cushing's disease : From cells, in vivo transgenic models to human pituitary organoids.Pituitary · 2025Review
- Update on the Role of Glucocorticoid Signaling in Osteoblasts and Bone Marrow Adipocytes During Aging.Current osteoporosis reports · 2023Review
- Gene Mutations in Cushing's Syndrome.Molecular syndromology · 2023Review
- Preclinical Models of Neuroendocrine Neoplasia.Cancers · 2022Review
- Metformin treatment confers protection of the optic nerve following photoreceptor degeneration.Anatomy & cell biology · 2021Article
- Monitoring type 2 diabetes from volatile faecal metabolome in Cushing's syndrome and single Afmid mouse models via a longitudinal study.Scientific reports · 2019Article
- Regulation of sclerostin in glucocorticoid-induced osteoporosis (GIO) in mice and humans.Endocrine connections · 2019Article
- Sost Haploinsufficiency Provokes Peracute Lethal Cardiac Tamponade without Rescuing the Osteopenia in a Mouse Model of Excess Glucocorticoids.The American journal of pathology · 2019Article
- Bone matrix development in steroid-induced osteoporosis is associated with a consistently reduced fibrillar stiffness linked to altered bone mineral quality.Acta biomaterialia · 2018Article
- The CRF Family of Neuropeptides and their Receptors - Mediators of the Central Stress Response.Current molecular pharmacology · 2018Review
- Article
- Mutant Mice With Calcium-Sensing Receptor Activation Have Hyperglycemia That Is Rectified by Calcilytic Therapy.Endocrinology · 2017Article
- Article
- GJCI insight · 2017Article
- Multiscale alterations in bone matrix quality increased fragility in steroid induced osteoporosis.Bone · 2016Article
- Animal models of pituitary neoplasia.Molecular and cellular endocrinology · 2016Review
- Article
- Dissection of glucocorticoid receptor-mediated inhibition of the hypothalamic-pituitary-adrenal axis by gene targeting in mice.Frontiers in neuroendocrinology · 2015Review
Corrections and comments
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Authors and funding
16 authors at 10 institutions in 2 countries.
Funding
Abstract
Cushing's syndrome, which is characterized by excessive circulating glucocorticoid concentrations, may be due to ACTH-dependent or -independent causes that include anterior pituitary and adrenal cortical tumors, respectively. ACTH secretion is stimulated by CRH, and we report a mouse model for Cushing's syndrome due to an N-ethyl-N-nitrosourea (ENU) induced Crh mutation at -120 bp of the promoter region, which significantly increased luciferase reporter activity and was thus a gain-of-function mutation. Crh(-120/+) mice, when compared with wild-type littermates, had obesity, muscle wasting, thin skin, hair loss, and elevated plasma and urinary concentrations of corticosterone. In addition, Crh(-120/+) mice had hyperglycemia, hyperfructosaminemia, hyperinsulinemia, hypercholesterolemia, hypertriglyceridemia, and hyperleptinemia but normal adiponectin. Crh(-120/+) mice also had low bone mineral density, hypercalcemia, hypercalciuria, and decreased concentrations of plasma PTH and osteocalcin. Bone histomorphometry revealed Crh(-120/+) mice to have significant reductions in mineralizing surface area, mineral apposition, bone formation rates, osteoblast number, and the percentage of corticoendosteal bone covered by osteoblasts, which was accompanied by an increase in adipocytes in the bone marrow. Thus, a mouse model for Cushing's syndrome has been established, and this will help in further elucidating the pathophysiological effects of glucocorticoid excess and in evaluating treatments for corticosteroid-induced osteoporosis.
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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.