Cell Death in Chondrocytes, Osteoblasts, and Osteocytes.
Cell Death in Chondrocytes, Osteoblasts, and Osteocytes.
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DOI：
10.3390/ijms17122045
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发表时间：
2016-12-06
影响因子：
5.6
通讯作者：
Komori T
中科院分区：
文献类型：
--
作者：
Komori T
骨骼成分细胞（包括软骨细胞、成骨细胞和骨细胞）中的细胞死亡在骨骼发育、维持和修复以及骨关节炎和骨质疏松症的发病机制中起作用。软骨细胞的增殖、分化和凋亡是软骨内骨化的重要步骤。虽然P53和Rb的失活参与了骨肉瘤的发病机制，但p53的缺失和Rb的失活不足以增强软骨细胞的增殖，表明软骨细胞中存在多种抑制肉瘤发生的机制。机械损伤和软骨细胞死亡通过释放软骨相关分子模式（DAMPs）诱导的炎症过程参与创伤后骨关节炎的发病机制。BCLXL的过表达增加了具有正常结构的骨体积，并通过抑制成骨细胞凋亡在衰老过程中维持骨。p53抑制成骨细胞增殖并增强成骨细胞凋亡，从而减少骨形成，但也通过Akt-FoxOs途径对成骨细胞分化发挥积极作用。凋亡骨细胞从泛连接蛋白1通道释放ATP，ATP诱导核因子κ-B配体受体激活剂（Rankl）表达和破骨细胞生成。骨细胞死亡最终导致坏死; DAMP被释放到骨表面并促进促炎细胞因子的产生，其诱导Rankl表达，并且破骨细胞生成进一步增强。
Cell death in skeletal component cells, including chondrocytes, osteoblasts, and osteocytes, plays roles in skeletal development, maintenance, and repair as well as in the pathogenesis of osteoarthritis and osteoporosis. Chondrocyte proliferation, differentiation, and apoptosis are important steps for endochondral ossification. Although the inactivation of P53 and RB is involved in the pathogenesis of osteosarcomas, the deletion of p53 and inactivation of Rb are insufficient to enhance chondrocyte proliferation, indicating the presence of multiple inhibitory mechanisms against sarcomagenesis in chondrocytes. The inflammatory processes induced by mechanical injury and chondrocyte death through the release of danger-associated molecular patterns (DAMPs) are involved in the pathogenesis of posttraumatic osteoarthritis. The overexpression of BCLXL increases bone volume with a normal structure and maintains bone during aging by inhibiting osteoblast apoptosis. p53 inhibits osteoblast proliferation and enhances osteoblast apoptosis, thereby reducing bone formation, but also exerts positive effects on osteoblast differentiation through the Akt–FoxOs pathway. Apoptotic osteocytes release ATP, which induces the receptor activator of nuclear factor κ-B ligand (Rankl) expression and osteoclastogenesis, from pannexin 1 channels. Osteocyte death ultimately results in necrosis; DAMPs are released to the bone surface and promote the production of proinflammatory cytokines, which induce Rankl expression, and osteoclastogenesis is further enhanced.
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影响因子：
29
作者：
Ambrogini E;Almeida M;Martin-Millan M;Paik JH;Depinho RA;Han L;Goellner J;Weinstein RS;Jilka RL;O'Brien CA;Manolagas SC
通讯作者：
Manolagas SC
DOI：
10.1002/jbmr.2740
发表时间：
2016-04
期刊：
Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research
影响因子：
--
作者：
Cheung WY;Fritton JC;Morgan SA;Seref-Ferlengez Z;Basta-Pljakic J;Thi MM;Suadicani SO;Spray DC;Majeska RJ;Schaffler MB
通讯作者：
Schaffler MB
影响因子：
6.2
作者：
Bivi, Nicoletta;Condon, Keith W.;Allen, Matthew R.;Farlow, Nathan;Passeri, Giovanni;Brun, Lucas R.;Rhee, Yumie;Bellido, Teresita;Plotkin, Lilian I.
通讯作者：
Plotkin, Lilian I.
影响因子：
4.8
作者：
Calbó, J;Parreño, M;Graña, X
通讯作者：
Graña, X
影响因子：
7
作者：
Dang, A. C.;Warren, A. P.;Kim, H. T.
通讯作者：
Kim, H. T.