An Integrated View of Stressors as Causative Agents in OA Pathogenesis.
An Integrated View of Stressors as Causative Agents in OA Pathogenesis.
复制标题
应力源作为OA发病机理中的致病剂的综合视图。
DOI：
10.3390/biom13050721
复制
发表时间：
2023-04-22
期刊：
影响因子：
5.5
通讯作者：
中科院分区：
文献类型：
--
作者：
体内的细胞暴露于动态的外部和内部环境，其中许多会导致细胞损伤。细胞对这种损伤的反应，广义上称为应激反应，旨在促进生存和修复或消除损伤。然而，并不是所有的损伤都可以修复，有时甚至更糟的是，压力反应会使系统本身负担过重，进一步恶化稳态并导致其丧失。衰老表型被认为是累积的细胞损伤和修复缺陷的表现。这在关节的主要细胞类型（关节软骨细胞）中尤其明显。关节软骨细胞不断面临压力源的挑战，包括机械过载，氧化，DNA损伤，蛋白质稳态应激和代谢失衡。关节软骨细胞上应力积累的结果是异常的有丝分裂和分化、有缺陷的细胞外基质产生和周转、细胞衰老和细胞死亡。关节中应力诱导的软骨细胞功能障碍的最严重形式是骨关节炎（OA）。在这里，我们总结了对关节软骨细胞的应激细胞效应的研究，并证明了分子效应的压力通路连接放大关节功能障碍和OA的发展。
Cells in the body are exposed to dynamic external and internal environments, many of which cause cell damage. The cell’s response to this damage, broadly called the stress response, is meant to promote survival and repair or remove damage. However, not all damage can be repaired, and sometimes, even worse, the stress response can overtax the system itself, further aggravating homeostasis and leading to its loss. Aging phenotypes are considered a manifestation of accumulated cellular damage and defective repair. This is particularly apparent in the primary cell type of the articular joint, the articular chondrocytes. Articular chondrocytes are constantly facing the challenge of stressors, including mechanical overloading, oxidation, DNA damage, proteostatic stress, and metabolic imbalance. The consequence of the accumulation of stress on articular chondrocytes is aberrant mitogenesis and differentiation, defective extracellular matrix production and turnover, cellular senescence, and cell death. The most severe form of stress-induced chondrocyte dysfunction in the joints is osteoarthritis (OA). Here, we summarize studies on the cellular effects of stressors on articular chondrocytes and demonstrate that the molecular effectors of the stress pathways connect to amplify articular joint dysfunction and OA development.
登录
查看更多内容
ERCC1 通过调节细胞凋亡和细胞衰老参与骨关节炎的发病机制。
影响因子：
2.8
作者：
Takayama, Koji;Kawakami, Yohei;Lee, Sahnghoon;Greco, Nick;Lavasani, Mitra;Mifune, Yutaka;Cummins, James H.;Yurube, Takashi;Kuroda, Ryosuke;Kurosaka, Masahiro;Fu, Freddie H.;Huard, Johnny
通讯作者：
Huard, Johnny
DOI：
10.1152/ajpheart.00717.2011
发表时间：
2012-02-01
影响因子：
4.8
作者：
Bubolz, Aaron H.;Mendoza, Suelhem A.;Zhang, David X.
通讯作者：
Zhang, David X.
影响因子：
7.8
作者：
通讯作者：
--
影响因子：
4.8
作者：
Collins, John A.;Wood, Scott T.;Loeser, Richard F.
通讯作者：
Loeser, Richard F.
影响因子：
7
作者：
Copp ME;Flanders MC;Gagliardi R;Gilbertie JM;Sessions GA;Chubinskaya S;Loeser RF;Schnabel LV;Diekman BO
通讯作者：
Diekman BO