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Molecular and Cellular Mechanisms of Intervertebral Disc Disease

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 31 December 2024 | Viewed by 1331

Special Issue Editor


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Guest Editor
1. The Orthopaedic Research Laboratory, Research Institute of the McGill University Health Centre, Montreal, QC, Canada
2. Department of Surgery, Division of Orthopaedics, McGill University, Montreal, QC, Canada
3. The McGill Scoliosis and Spine Group, McGill University Health Centre, Montreal, QC, Canada
Interests: cellular mechanisms in physiological and pathological conditions; favoring the development of new therapeutic agents capable of treating musculoskeletal pathologies
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue, titled “Molecular and Cellular Mechanisms of Intervertebral Disc Disease”, aims to explore recent advancements and comprehensive reviews in intervertebral disc biology, particularly focusing on disc degeneration and aging. Experimental research papers, up-to-date review articles, and insightful commentaries are invited.

The intervertebral disc (IVD) is a critical component of the spine, comprising a complex structure involving the extracellular matrix (ECM), predominantly composed of collagen and proteoglycans. IVD degeneration, a prevalent condition, involves intricate molecular and cellular mechanisms. Several factors such as age, genetic predisposition, and oxidative and mechanical stress have been suggested to contribute to the initiation and progression of IVD degeneration. Current treatments can only reduce the severity of the symptoms, but they cannot prevent the degeneration from progressing. Research topics of interest include, but are not limited to, the following:

  • Molecular mechanisms underlying disc degeneration, including cellular senescence, apoptosis, ferroptosis, necrosis, inflammation, and oxidative stress.
  • Cellular processes such as ECM remodeling mediated by matrix metalloproteinases (MMPs) and their inhibitors.
  • The role of cytokines and growth factors in disc health and disease.
  • Mechanisms influencing disc aging, nutrition, and mechanical integrity.
  • Biomarkers for assessing disc degeneration progression and therapeutic response.
  • Advances in understanding disc herniation and potential strategies for disc regeneration.

Contributions exploring new therapeutic avenues, including molecular targets, regenerative approaches, and innovative diagnostic techniques, are encouraged. Additionally, studies utilizing animal models and clinical trials aimed at validating therapeutic strategies for disc degeneration are welcome.

We look forward to your valuable contributions to this Special Issue.

Dr. Hosni Cherif
Guest Editor

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Keywords

  • intervertebral disc
  • disc degeneration
  • low back pain
  • disc aging
  • disc herniation
  • disc regeneration
  • inflammation
  • extracellular matrix
  • collagen
  • proteoglycans
  • matrix metalloproteinases (MMPs)
  • senescence
  • quiescence
  • apoptosis
  • oxidative stress
  • senotherapeutics
  • cytokines
  • growth factors

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Published Papers (1 paper)

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Research

13 pages, 11999 KiB  
Article
The Role of the Bone Morphogenetic Protein Antagonist Noggin in Nucleus Pulposus Intervertebral Disc Cells
by Shuimu Chen, Sebastian Bigdon, Carsten Riether, Xiaochi Ma, Xiaoyi Niu, Sonja Häckel, Zhen Li and Benjamin Gantenbein
Int. J. Mol. Sci. 2024, 25(21), 11803; https://doi.org/10.3390/ijms252111803 - 2 Nov 2024
Viewed by 1039
Abstract
Low back pain (LBP) is a significant global health issue, contributing to disability and socioeconomic burdens worldwide. The degeneration of the human intervertebral disc (IVD) is a critical factor in the pathogenesis of LBP. Recent studies have emphasized the significance of a specific [...] Read more.
Low back pain (LBP) is a significant global health issue, contributing to disability and socioeconomic burdens worldwide. The degeneration of the human intervertebral disc (IVD) is a critical factor in the pathogenesis of LBP. Recent studies have emphasized the significance of a specific set of genes and extracellular matrix (ECM) in IVD health. In particular, Noggin has emerged as a critical gene due to its high expression levels in healthy nucleus pulposus cells (NPCs) observed in our previous research. In this study, it was hypothesized that decreased Noggin expression in NPCs is associated with IVD degeneration and contributes to LBP development. A lentivirus-mediated RNAi was applied to knock down Noggin expression in primary NPCs from six human donors. The NPCs after transduction were evaluated through cell viability analysis, XTT assay, and cell apoptosis analyses. After two weeks, a colony formation assay was used to examine the anchor-independent growth ability of transduced cells. At the transcript level, anabolic and catabolic markers were quantified using RT-qPCR. The results demonstrated that lentivirus-mediated downregulation of Noggin significantly inhibited cell proliferation, reduced cell viability, and suppressed colony formation, while inducing apoptosis in human NPCs in vitro. Notably, it disrupted cellular anabolic processes and promoted catabolic activity in human NPCs post-transduction. Our findings indicated that the degeneration of human IVD is possibly related to decreased Noggin expression in NPCs. This research provides valuable insights into the role of Noggin in IVD homeostasis and its implications in LBP treatment. Full article
(This article belongs to the Special Issue Molecular and Cellular Mechanisms of Intervertebral Disc Disease)
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