4.7 Review

The potential role of melatonin in retarding intervertebral disc ageing and degeneration: A systematic review

期刊

AGEING RESEARCH REVIEWS
卷 70, 期 -, 页码 -

出版社

ELSEVIER IRELAND LTD
DOI: 10.1016/j.arr.2021.101394

关键词

Ageing; Intervertebral disc degeneration; Melatonin; Low back pain; Nucleus pulposus cells

资金

  1. National Natural Science Foundation of China [81974348, 81772391]

向作者/读者索取更多资源

Research has shown that melatonin can inhibit the development of intervertebral disc degeneration in various ways, playing an important role in maintaining the structural integrity of intervertebral discs and promoting anti-stress abilities and matrix synthesis.
Intervertebral disc degeneration (IDD) is a common degenerative disease of the musculoskeletal system that develops with age. It is regarded as the main cause of chronic low back pain in the elderly. IDD has various causes, including ageing, mechanical overloading, and nutritional deficiency. Melatonin is a pleiotropic indole hormone secreted by the pineal gland and plays an important role in resisting various degenerative diseases. The serum levels of melatonin decline with age and are reported to be negatively correlated with the symptomatic and histopathological scores of IDD. In vivo studies have shown that exogenous administration of melatonin could maintain the structural integrity of the intervertebral disc and inhibit the development of IDD. Mechanistically, by interacting with its membrane or intracellular receptors, melatonin can promote autophagic flux, scavenge free radicals, inhibit the release of pro-inflammatory factors, and block apoptotic pathways, thereby enhancing anti-stress abilities and matrix anabolism in different types of disc cells. Therefore, melatonin supplementation may be a promising therapeutic strategy for IDD. This review aimed to summarize the latest findings regarding the therapeutic potential of melatonin in IDD.

作者

我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。

评论

主要评分

4.7
评分不足

次要评分

新颖性
-
重要性
-
科学严谨性
-
评价这篇论文

推荐

暂无数据
暂无数据