The maintenance of spinal stability depends on the coordinated movement of the paraspinal muscles and the intervertebral discs. The structure and function disorder of them might contribute to intervertebral disc disease (IDD), which arises from a number of disorders including intervertebral disc prolapse, lumbar spondylolisthesis, spinalstenosis, scoliosis, and cervical spondylopathy, followed by triggering low back pain (LBP), causing a tremendous economic and social impact around the world. Intervertebral disc and paraspinal muscle degeneration (PMD) is the pathological basis of IDD. Sagittal imbalance can promote the degeneration of the paraspinal muscles (such as multifidus and erector spinae, etc.) and lead to IDD, while IDD can also provoke PMD. IDD often starts from the nucleus pulposus (NP), and the maintenance of NP physiological function depends on the homeostasis of cells, extracellular matrix (ECM), redox, and inflammation. Under various unfavorable factors, NP cells first secrete pro-inflammatory factors, then induce the inflammatory cell death and release inflammatory factors. Pro-inflammatory factors further promote ECM degradation and IDD. Nevertheless, the understanding of the molecular mechanism of pro-inflammatory factors-mediated NPCs death, ECM metabolism, oxidative stress, and inflammatory response is still very limited. In addition, the clinical treatment of IDD can only alleviate or relieve clinical symptoms, and neither can fundamentally block the vicious circle process of IDD. As a result, new therapeutic strategies are required urgently. Therapies targeting genes or non-coding RNAs can postpone or even reverse intervertebral disc degeneration at the gene level by inhibiting inflammatory cell death and inflammatory response, which can be an effective strategy or treatment for IDD.
The purpose of this Research Topic is to provide a platform for researchers to investigate the pathological mechanism of IDD and elucidate the potential roles and regulatory mechanisms of inflammatory cell death and inflammatory response during intervertebral disc degeneration, as well as the mediation of genes and non-coding RNAs therein effect.
We welcome Original Research, Clinical Trial, and Review papers concerning the following subtopics, including but not limited to:
• Potential therapeutic molecules to treat IDD;
• The role of sagittal imbalance in PMD as well as the relationship between intervertebral disc degeneration and PMD;
• The potential roles and regulatory mechanisms of inflammatory cell death and inflammatory response in the occurrence and progression of IDD;
• Bioinformatical analysis of the underlying mechanisms related to IDD, including but not limited to differential gene or non-coding RNAs expression, Go and KEGG pathway enrichment analysis, and module analyses for protein-protein interaction (PPI) network;
• Genes or non-coding RNAs mediate IDD by regulating inflammatory cell death and inflammatory responses;
• Specific molecular signaling pathways related to IDD
The maintenance of spinal stability depends on the coordinated movement of the paraspinal muscles and the intervertebral discs. The structure and function disorder of them might contribute to intervertebral disc disease (IDD), which arises from a number of disorders including intervertebral disc prolapse, lumbar spondylolisthesis, spinalstenosis, scoliosis, and cervical spondylopathy, followed by triggering low back pain (LBP), causing a tremendous economic and social impact around the world. Intervertebral disc and paraspinal muscle degeneration (PMD) is the pathological basis of IDD. Sagittal imbalance can promote the degeneration of the paraspinal muscles (such as multifidus and erector spinae, etc.) and lead to IDD, while IDD can also provoke PMD. IDD often starts from the nucleus pulposus (NP), and the maintenance of NP physiological function depends on the homeostasis of cells, extracellular matrix (ECM), redox, and inflammation. Under various unfavorable factors, NP cells first secrete pro-inflammatory factors, then induce the inflammatory cell death and release inflammatory factors. Pro-inflammatory factors further promote ECM degradation and IDD. Nevertheless, the understanding of the molecular mechanism of pro-inflammatory factors-mediated NPCs death, ECM metabolism, oxidative stress, and inflammatory response is still very limited. In addition, the clinical treatment of IDD can only alleviate or relieve clinical symptoms, and neither can fundamentally block the vicious circle process of IDD. As a result, new therapeutic strategies are required urgently. Therapies targeting genes or non-coding RNAs can postpone or even reverse intervertebral disc degeneration at the gene level by inhibiting inflammatory cell death and inflammatory response, which can be an effective strategy or treatment for IDD.
The purpose of this Research Topic is to provide a platform for researchers to investigate the pathological mechanism of IDD and elucidate the potential roles and regulatory mechanisms of inflammatory cell death and inflammatory response during intervertebral disc degeneration, as well as the mediation of genes and non-coding RNAs therein effect.
We welcome Original Research, Clinical Trial, and Review papers concerning the following subtopics, including but not limited to:
• Potential therapeutic molecules to treat IDD;
• The role of sagittal imbalance in PMD as well as the relationship between intervertebral disc degeneration and PMD;
• The potential roles and regulatory mechanisms of inflammatory cell death and inflammatory response in the occurrence and progression of IDD;
• Bioinformatical analysis of the underlying mechanisms related to IDD, including but not limited to differential gene or non-coding RNAs expression, Go and KEGG pathway enrichment analysis, and module analyses for protein-protein interaction (PPI) network;
• Genes or non-coding RNAs mediate IDD by regulating inflammatory cell death and inflammatory responses;
• Specific molecular signaling pathways related to IDD
