衰老
河马信号通路
活性氧
氧化应激
细胞生物学
生物
体内
细胞
癌症研究
信号转导
内分泌学
生物化学
遗传学
作者
Hu Tao,Zhan Shi,Yuan Sun,Hui Feng,Yuluo Rong,Jia Wang,Liang Wang,Wenbin Xu,Feng Zhang,Wenzhi Zhang
出处
期刊:American Journal of Physiology-cell Physiology
[American Physiological Society]
日期:2023-12-18
被引量:1
标识
DOI:10.1152/ajpcell.00571.2023
摘要
Nucleus pulposus cell (NPC) senescence is a major cause of intervertebral disc degeneration (IVDD). Oxidative stress and reactive oxygen species (ROS) play critical roles in regulating cell senescence. Selenophosphate synthetase 1 (SEPHS1) was reported to play an important role in mitigating oxidative stress in an osteoarthritis model by reducing the production of ROS, thereby, delaying the occurrence and development of osteoarthritis. In this study, we explored the, hitherto unknown, role of SEPHS1 in IVDD in vitro and in vivo using an interleukin-1 beta (IL-1β)-induced NPC senescence model and a rat needle puncture IVDD model, respectively. SEPHS1 delayed NPC senescence in vitro by reducing ROS production. Age-related dysfunction was also ameliorated by the overexpression of SEPHS1 and inhibition of the Hippo-Yap/Taz signaling pathway. In vivo experiments revealed that the overexpression of SEPHS1 and inhibition of Hippo-Yap/Taz alleviated IVDD in rats. Moreover, a selenium-deficient diet and lack of SEPHS1 synergistically aggravated IVDD progression. Taken together, our results demonstrate that SEPHS1 plays a significant role in NPC senescence. Overexpression of SEPHS1 and inhibition of Hippo-Yap/Taz can delay NPC senescence, restore the balance of extracellular matrix metabolism, and attenuate IVDD. SEPHS1 could be a promising therapeutic target for IVDD.
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