Send to

Choose Destination
Cell Prolif. 2018 Oct;51(5):e12483. doi: 10.1111/cpr.12483. Epub 2018 Jul 24.

Long non-coding RNAs in nucleus pulposus cell function and intervertebral disc degeneration.

Author information

Department of Orthopaedic Surgery, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.
Department of Orthopedic Surgery, Beijing Jishuitan Hospital, Fourth Clinical College of Peking University, Jishuitan Orthopaedic College of Tsinghua University, Beijing, China.
Department of Medicine and Therapeutics, The Chinese University of Hong Kong, Hong Kong, China.
Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong, Hong Kong, China.
Department of Anaesthesia and Intensive Care and State Key Laboratory of Digestive Diseases, The Chinese University of Hong Kong, Hong Kong, China.


Intervertebral disc degeneration (IDD) is the major cause of low back pain which incurs a significant public-health and economic burden. The aetiology of IDD is complex, with developmental, genetic, biomechanical and biochemical factors contributing to the disease development. Deregulated phenotypes of nucleus pulposus cells, including aberrant differentiation, apoptosis, proliferation and extracellular matrix deposition, are involved in the initiation and progression of IDD. Non-coding RNAs, including long non-coding RNAs (lncRNAs), have recently been identified as important regulators of gene expression. Research into their roles in IDD has been very active over the past 5 years. Our review summarizes current research regarding the roles of deregulated lncRNAs (eg, RP11-296A18.3, TUG1, HCG18) in modulating nucleus pulposus cell functions in IDD. These exciting findings suggest that specific modulation of lncRNAs or their downstream signalling pathways might be an attractive approach for developing novel therapeutics for IDD.


cell death; extracellular matrix; low back pain; pathogenesis; prolapsed disc

[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Wiley
Loading ...
Support Center