Intervertebral Disc Degeneration: Mechanisms and Therapeutics

Intervertebral disc (IVD) degeneration is a critical health challenge, leading to a variety of spine diseases including intervertebral disc herniation, spinal stenosis, instability, etc., which contribute largely to the disability among orthopaedic patients. Although large strides have been made in understanding IVD degeneration, and previous studies in human and experimental animal models have demonstrated that cellular activities such as excessive apoptosis and autophagy play a key role during IVD progression, more remains to be further explored due to the changes in the biomechanics of the intervertebral disc, the decrease in intervertebral height, the degeneration of the cartilage endplate, the degradation of the extracellular matrix, and an increase in inflammatory factors. For example, what are the mechanisms and molecular signaling pathways that cause IVD dysfunction? What are the mechanisms underlying neuropathic pain related to disc degeneration?

This Research Topic focuses on cellular and signaling pathway changes and mechanisms of intervertebral disc degeneration. We are also open to studies regarding potential molecular therapies and degeneration-related pain. Therefore, we welcome reviews (including mini-reviews) and original studies that deal with but are not limited to the following:
• Cellular mechanisms in IVD degeneration and related diseases, including cell proliferation, differentiation, metabolism, apoptosis, autophagy, endoplasmic reticulum stress, and cell signal transduction, gene expression and regulation;
• Specific molecular pathways that induce IVD degeneration and ageing;
• Potential therapeutic molecules to attenuate the progression of IVD cells degeneration and related diseases including discogenic neuropathic pain and its mechanisms;
• Novel or potential diagnostics and prognosis for IVD degeneration-related diseases;
• Bioengineering therapeutics for IVD degenerative diseases, including biomaterials and stem/progenitor cells;
• IVD degeneration models induced by apoptosis or autophagy of IVD cells.