氧化应激在椎间盘细胞衰老中的作用。
The role of oxidative stress in intervertebral disc cellular senescence.
机构信息
Department of Orthopedic Surgery, Beijing Chao-Yang Hospital, Capital Medical University, Beijing, China.
出版信息
Front Endocrinol (Lausanne). 2022 Dec 6;13:1038171. doi: 10.3389/fendo.2022.1038171. eCollection 2022.
With the aggravation of social aging and the increase in work intensity, the prevalence of spinal degenerative diseases caused by intervertebral disc degeneration(IDD)has increased yearly, which has driven a heavy economic burden on patients and society. It is well known that IDD is associated with cell damage and degradation of the extracellular matrix. In recent years, it has been found that IDD is induced by various mechanisms (e.g., genetic, mechanical, and exposure). Increasing evidence shows that oxidative stress is a vital activation mechanism of IDD. Reactive oxygen species (ROS) and reactive nitrogen species (RNS) could regulate matrix metabolism, proinflammatory phenotype, apoptosis, autophagy, and aging of intervertebral disc cells. However, up to now, our understanding of a series of pathophysiological mechanisms of oxidative stress involved in the occurrence, development, and treatment of IDD is still limited. In this review, we discussed the oxidative stress through its mechanisms in accelerating IDD and some antioxidant treatment measures for IDD.
随着社会老龄化的加剧和工作强度的增加,由椎间盘退行性变(IDD)引起的脊柱退行性疾病的患病率逐年增加,给患者和社会带来了沉重的经济负担。众所周知,IDD 与细胞损伤和细胞外基质降解有关。近年来,人们发现 IDD 是由多种机制(如遗传、机械和暴露)引起的。越来越多的证据表明,氧化应激是 IDD 的一个重要激活机制。活性氧(ROS)和活性氮(RNS)可以调节基质代谢、前炎性表型、细胞凋亡、自噬和椎间盘细胞衰老。然而,到目前为止,我们对氧化应激在 IDD 发生、发展和治疗中的一系列病理生理机制的理解仍然有限。在这篇综述中,我们讨论了氧化应激通过其机制加速 IDD 以及一些抗氧化治疗 IDD 的措施。