Glucocorticoid induced osteoporosis (GIO) is the most frequent form of drug induced osteoporosis. Glucocorticoids affect osteoblastogenesis, osteoclastogenesis and promote the apoptosis of osteoblasts and osteocytes. A decrease of bone mineral density has been described in several pediatric diseases that require glucocorticoids, both as long-term replacement therapy, such as Congenital Adrenal Hyperplasia, and as treatment of acute phase or relapses, such as asthma, juvenile rheumatoid arthritis, inflammatory bowel diseases, systemic lupus erythematosus, organ transplantation and Steroid Sensitive Nephrotic Syndrome. The increasing number of children with GIO and at risk of fractures reflects the complex nature of this condition, and the need of development of anti-osteoporotic drugs. In this review, we focus on the mechanisms of GIO in some pediatric diseases and on treatment of osteoporosis. We also report data on new signaling pathways as potential targets for future anti-osteoporotic drugs.
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http://dx.doi.org/10.1586/17446651.2014.936384 | DOI Listing |
Int Urol Nephrol
January 2025
Nephrology, Dialysis and Kidney Transplant Unit, IRCCS Azienda Ospedaliero-Universitaria di Bologna, Bologna, Italy.
Introduction: Kidney transplantation is the preferred treatment for end-stage kidney disease (ESKD), enhancing survival and quality of life. However, kidney transplant recipients (KTRs) are at high risk for bone disorders, particularly low bone turnover disease, which increases fracture risk. Teriparatide, an anabolic agent, may provide a beneficial treatment option for these patients.
View Article and Find Full Text PDFInt Immunopharmacol
January 2025
Department of Endocrinology, Sichuan Provincial People's Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, Sichuan 610072, China. Electronic address:
The immune-responsive gene 1 (IRG1) protein plays a role in various pathological processes by connecting cellular metabolism to a range of cellular activities through the production of itaconate. Recent studies have highlighted the significance of IRG1 and itaconate in bone metabolism and homeostasis. However, the precise role of IRG1 in osteoporosis remains inadequately documented.
View Article and Find Full Text PDFMol Biol Rep
January 2025
Medical Sociology and Psychobiology, Department of Health and Physical Activity, University of Potsdam, 14469, Potsdam, Germany.
Background: Depression constitutes a risk factor for osteoporosis, but underlying molecular and cellular mechanisms are not fully understood. MiRNAs influence gene expression and are carried by extracellular vesicles (EV), affecting cell-cell communication.
Aims: (1) Identify the difference in miRNA expression between depressed patients and healthy controls; (2) Analyze associations of these miRNAs with bone turnover markers; (3) Analyze target genes of differentially regulated miRNAs and predict associated pathways regarding depression and bone metabolism.
Cochrane Database Syst Rev
January 2025
Department of Medicine, Faculty of Medicine, University of Ottawa, Ottawa, Canada.
Rationale: Osteoporosis is an abnormal reduction in bone mass and bone deterioration, leading to increased fracture risk. Alendronate belongs to the bisphosphonate class of drugs, which inhibit bone resorption by interfering with the activity of osteoclasts (bone cells that break down bone tissue). This is an update of a Cochrane review first published in 2008.
View Article and Find Full Text PDFFront Genet
January 2025
Department of Orthopedics, First Hospital of Jiaxing, Jiaxing, China.
Background: Ferroptosis-related genes have been reported to play important roles in many diseases, but their molecular mechanisms in osteoporosis have not been elucidated.
Methods: Based on two independent GEO datasets (GSE35956 and GSE35958), and GSE35959 as the validation dataset, we comprehensively elucidated the pathological mechanism of ferroptosis-related genes in osteoporosis by GO analyses, KEGG analyses and a PPI network. Then, We used Western Blot (WB) and Quantitative real-time polymerase chain reaction (qPCR) to verify the expression level of KMT2D, a ferroptosis-related hub gene, in clinical samples.
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