A critical relationship between bone and fat: the role of bone marrow adipose-derived RANKL in bone metabolism
Autor: | Masahiro Onji, Nicolas Werschler, Josef M. Penninger |
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Rok vydání: | 2021 |
Předmět: |
Adult
medicine.medical_specialty Osteoporosis Osteoclasts Adipose tissue Mice Transgenic Biochemistry Bone and Bones Bone remodeling Mice 03 medical and health sciences 0302 clinical medicine Bone Marrow Internal medicine Clinical investigation Genetics medicine Adipocytes Animals Humans News & Views Molecular Biology of Disease Bone Resorption Musculoskeletal System Molecular Biology 030304 developmental biology 0303 health sciences biology business.industry RANK Ligand Articles medicine.disease Pathophysiology Endocrinology medicine.anatomical_structure Adipose Tissue RANKL biology.protein Adiponectin Bone Remodeling Bone marrow business 030217 neurology & neurosurgery Signal Transduction |
Zdroj: | EMBO Rep EMBO Reports |
ISSN: | 1469-3178 |
Popis: | Recent studies have unveiled unique functions of the bone marrow adipose tissue (BMAT), which represent over 10% of the total adipose tissue mass in healthy adults. Increasing evidence is emerging as to how BMAT deposition and osteoporosis are linked under normal and pathophysiological conditions, which is opening up novel treatment avenues. However, the means by which bone marrow adipocytes (BMAs) regulate bone remodeling and their involvement in osteoporosis remained unknown. A study in this issue of EMBO Reports (Hu et al, 2021) and a study in Journal of Clinical Investigation (Yu et al, 2021) reports independently that BMA‐derived RANKL regulates osteoclastogenesis and bone remodeling, indicating that excessive RANKL generated by BMAs is an underlying cause for osteoporosis. The receptor activator of NF‐κB (RANK) and its ligand RANKL regulate osteoclast development and bone metabolism. Two recent studies provide evidence for a critical role of bone marrow adipocyte‐derived RANKL in osteoclastogenesis and bone remodeling. |
Databáze: | OpenAIRE |
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