منابع مشابه
RANK ligand and osteoprotegerin in myeloma bone disease.
Myeloma bone disease is due to interactions of myeloma cells with the bone marrow microenvironment, and is associated with pathologic fractures, neurologic symptoms and hypercalcemia. Adjacent to myeloma cells, the formation and activation of osteoclasts is increased, which results in enhanced bone resorption. The recent characterization of the essential cytokine of osteoclast cell biology, rec...
متن کاملPathophysiology of RANK ligand (RANKL) and osteoprotegerin (OPG).
Receptor activator of nuclear factorκ B ligand (RANKL) is a membrane-bound peptide of the tumor necrosis factor (TNF) ligand superfamily [14]. Rich sources of RANKL expression include T lymphocytes [12] and osteoblastic lineage cells [8]. In the presence of permissive concentrations of macrophage-colony stimulating factor (M-CSF), RANKL stimulates the differentiation, proliferation, fusion and ...
متن کاملDysregulated osteoprotegerin/RANK ligand/RANK axis in clinical and experimental heart failure.
BACKGROUND Persistent inflammation appears to play a role in the development of heart failure (HF). Osteoprotegerin (OPG), the receptor activator of nuclear factor-kappaB (RANK), and RANK ligand (RANKL) are newly discovered members of the tumor necrosis factor superfamily that are critical regulators in bone metabolism but appear also to be involved in immune responses. We hypothesized that the...
متن کاملRANK ligand and osteoprotegerin: paracrine regulators of bone metabolism and vascular function.
In 1997, investigators isolated a secreted glycoprotein that blocked osteoclast differentiation from precursor cells, prevented osteoporosis (decreased bone mass) when administered to ovariectomized rats, and resulted in osteopetrosis (increased bone mass) when overexpressed in transgenic mice. Since then, the isolation and characterization of the protein named osteoprotegerin (OPG) has stimula...
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ژورنال
عنوان ژورنال: Arteriosclerosis, Thrombosis, and Vascular Biology
سال: 2002
ISSN: 1079-5642,1524-4636
DOI: 10.1161/01.atv.0000012303.37971.da