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Bone metabolism is the basis for maintaining the normal physiological state of bone, and imbalance of bone metabolism can lead to a series of metabolic bone diseases. As a member of the IL-6 family, IL-11 acts primarily through the classical signaling pathway IL-11/Receptors, IL-11 (IL-11R)/Glycoprotein 130 (gp130). The regulatory role of IL-11 in bone metabolism has been found earlier, but mainly focuses on the effects on osteogenesis and osteoclasis. In recent years, more studies have focused on IL-11's roles and related mechanisms in different bone metabolism activities. IL-11 regulates osteoblasts, osteoclasts, BM stromal cells, adipose tissue-derived mesenchymal stem cells, and chondrocytes. It's involved in bone homeostasis, including osteogenesis, osteolysis, bone marrow (BM) hematopoiesis, BM adipogenesis, and bone metastasis. This review exams IL-11's role in pathology and bone tissue, the cytokines and pathways that regulate IL-11 expression, and the feedback regulations of these pathways.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10862480 | PMC |
http://dx.doi.org/10.3389/fendo.2023.1290130 | DOI Listing |
BMJ Open
March 2025
Department of Growth and Reproduction, Copenhagen University Hospital, Rigshospitalet, Copenhagen, Denmark
Introduction: Klinefelter syndrome (KS) is a genetic condition characterised by the presence of an extra X chromosome in males (47,XXY). KS is associated with various phenotypic characteristics in adult life, including infertility, hypogonadism and increased risk of type II diabetes, cardiovascular disease and osteoporosis. Additionally, individuals with KS often experience mental health challenges and functional impairments that significantly impact their quality of life.
View Article and Find Full Text PDFJoint Bone Spine
March 2025
School of Pharmacy, Tokyo University of Pharmacy and Life Sciences, Tokyo, Japan; Chiba Health Promotion Center, East Japan Railway Company, Chiba, Japan.
Elevated serum uric acid levels are the essential pathophysiology of gout. Although gout rarely develops in childhood, chronic persistent hyperuricemia can induce precipitation and deposition of sodium urate crystals, leading to the development of gout. Hyperuricemia is caused by increased uric acid production and/or decreased uric acid excretion capacity of the kidneys and/or intestinal tract.
View Article and Find Full Text PDFBone
March 2025
INICSA (CONICET-Universidad Nacional de Córdoba), Argentina; Cátedra de Bioquímica y Biología Molecular, Facultad de Ciencias Médicas, INICSA (CONICET-Universidad Nacional de Córdoba), Argentina. Electronic address:
Background: The decline in kidney function adversely affects mineral and bone disease, leading to decreased bone mass, increased fractures, and vascular calcifications (VC), particularly in advanced CKD stage 5. This study aimed to identify VC markers to eventually develop personalized therapeutic and preventive strategies in Argentina, where data is limited.
Methods: A prospective, observational study included 101 patients on dialysis or pre-dialysis, eligible for kidney transplant at the Private University Hospital of Córdoba from June 2019 to December 2020.
Drug Resist Updat
March 2025
Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, CA, USA; Cedars-Sinai Cancer Center, Los Angeles, CA, USA. Electronic address:
Aim: To investigate the role of CD105 in mediating drug resistance to EGFR-targeted therapy in non-small cell lung cancer (NSCLC).
Methods: Imaging mass cytometry was conducted on 66 NSCLC tumors, 44 of which had EGFR mutations. We correlated clinical variables, including overall survival, with CD105 (endoglin) expression, a co-receptor for bone morphogenetic protein (BMP) signaling.
J Bone Miner Res
March 2025
Division of Bone and Mineral Diseases, Washington University in St. Louis, MO, United States.
Background: A significant number of kidney transplant recipients have low BMD. We hypothesized that calcitriol administration over the first year post-transplantation would protect the cortical skeleton in recipients managed without corticosteroids by suppressing PTH and bone remodeling.
Methods: In this double-blind, placebo-controlled trial, 67 participants aged ≥18 years on corticosteroid-sparing immunosuppressive regimen were randomized to daily calcitriol 0.
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