作者: Toshihisa Komori
DOI: 10.3390/IJMS17122045
关键词:
摘要: Cell death in skeletal component cells, including chondrocytes, osteoblasts, and osteocytes, plays roles development, maintenance, repair as well the pathogenesis of osteoarthritis osteoporosis. Chondrocyte proliferation, differentiation, apoptosis are important steps for endochondral ossification. Although inactivation P53 RB is involved osteosarcomas, deletion p53 Rb insufficient to enhance chondrocyte indicating presence multiple inhibitory mechanisms against sarcomagenesis chondrocytes. The inflammatory processes induced by mechanical injury through release danger-associated molecular patterns (DAMPs) posttraumatic osteoarthritis. overexpression BCLXL increases bone volume with a normal structure maintains during aging inhibiting osteoblast apoptosis. inhibits proliferation enhances apoptosis, thereby reducing formation, but also exerts positive effects on differentiation Akt-FoxOs pathway. Apoptotic osteocytes ATP, which induces receptor activator nuclear factor κ-B ligand (Rankl) expression osteoclastogenesis, from pannexin 1 channels. Osteocyte ultimately results necrosis; DAMPs released surface promote production proinflammatory cytokines, induce Rankl expression, osteoclastogenesis further enhanced.