Intervertebral disc (IVD) degeneration, an important cause of discogenic lower back pain (LBP), has traditionally been thought to be an age-related process of the disc tissue caused by decreased proteoglycan content, eventually leading to decreased intervertebral height, endplate sclerosis and osteophyte formation. IVD degeneration can cause a variety of spinal diseases including lumbar disc herniation, lumbar spondylolisthesis, spinal stenosis, scoliosis, and cervical spondylopathy. Over the past decades, IVD degeneration-related diseases have been causing an enormous socio-economic burden and leading to low quality of life.

The process of IVD degeneration is complicated. Although the mechanism of IVD degeneration is not fully understood, altered mechanical loading, degradation of the extracellular matrix (ECM), increased secretion of inflammatory factors, excessive senescence, and aberrant apoptosis of IVD cells have proved to play important roles in the progression of IVD degeneration. Previous studies in humans and experimental animal models have well documented that oxidative stress and damage can result in excessive apoptosis and autophagy of IVD cells and further lead to IVD degeneration. However, the specific signalling pathways underlying the pathogenesis still remain elusive, making it very difficult to find potential therapeutics targeting that unclear mechanism.

This issue will mainly focus on four aspects.

1. The specific molecular pathways underlying oxidative stress-induced IVD degeneration and ageing.

2. Therapeutic molecules that attenuate the progression of IVD degeneration.

3. Biomaterials for IVD repair and regeneration.

4. Stem/ progenitor cells for IVD repair and regeneration.

Contributions with original research are extremely welcome if that would provide new insights for understanding the pathophysiological mechanism of oxidative damage-induced IVD degeneration and/or novel discovery of its diagnostics and therapeutics. Review articles (including mini-review) that help better understand the existing knowledge regarding the role of oxidative stress and related therapeutics are also welcome. In particular, three-dimensional culture and hypoxic culture of IVD cells are greatly encouraged.

Potential topics include but are not limited to the following:

• Oxidative stress in IVD degeneration and aging related diseases, including LBP, lumbar disc herniation, lumbar spondylolisthesis, spinal stenosis, scoliosis, and cervical spondylopathy
• Specific molecular pathways underlying oxidative stress-induced IVD degeneration and ageing
• Potential therapeutic molecules to attenuate the progression of IVD degeneration
• Novel or potential diagnostics and prognosis for IVD degeneration- related diseases
• Original research on potential medicinal plants are also welcome if the mechanism or molecular targets are also elucidated in treating IVD degeneration-related diseases
• Bioinformatical analysis of the underlying mechanisms related to oxidative stress-induced IVD degenerative diseases, including but not limited to differential gene expression, functional and pathway enrichment analyses, and module analyses for protein-protein interaction (PPI) network
• Bioengineering therapeutics for oxidative damage-induced IVD degenerative diseases, including biomaterials and stem/progenitor cells
• IVD degeneration models induced by oxidative damage, including in vivo, ex vivo, and in vitro models
• Meta-analysis of randomized controlled trials or primary clinical data used to evaluate the efficacy, or otherwise, of novel or potential therapeutics for IVD degeneration-related diseases