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Molecular Pathogenesis 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: 25 June 2024 | Viewed by 1427

Special Issue Editor

Department of Orthopedic Surgery, Rush University Medical Center, Chicago, IL 60012, USA
Interests: disc disease; pain mechanism; cell signaling; animal experiments; epigenetics; temporomandibular disease

Special Issue Information

Dear Colleagues,

Intervertebral disc diseases are chronic conditions, caused by several factors, which have still not been adequately understood or solved. Categories of these diseases include degenerative changes, subclinical or overt trauma, infectious lesions, inflammatory insults, metabolic disease, and tumors. Current strategies aim to halt or even reverse disc degeneration, restore physiologic disc function, and reduce pain. However, the intervertebral disc is a challenging tissue for regenerative and molecular approaches due to its low cellularity and the harsh microenvironment (e.g., high mechanical loads, low nutrition and oxygen supply, acidic pH), thus limiting the success of techniques that are commonly applied in other fields. Therefore, classical techniques that entail, for example, cells, biomaterials, and/or biological agents need to be modified such that they meet the specific requirements of disc diseases.

This Special Issue will focus on, but not be limited to: (1) the updated evidence regarding the epidemiology, pathophysiology and diagnosis intervertebral disc diseases; (2) biomaterial-based tissue engineering strategies; (3) the role of stem cell and exosomes for intervertebral disc diseases.

Dr. Chundo Oh
Guest Editor

Manuscript Submission Information

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Keywords

  • stem cells
  • cytokines
  • degenerative disc disease
  • disc degeneration
  • disc herniation
  • exosomes
  • genetics
  • genome engineering
  • inflammation
  • ion channels

Published Papers (1 paper)

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Research

16 pages, 12330 KiB  
Article
TMT-Based Proteomics Analysis of Senescent Nucleus Pulposus from Patients with Intervertebral Disc Degeneration
by Guangzhi Zhang, Lei Li, Zhili Yang, Cangyu Zhang and Xuewen Kang
Int. J. Mol. Sci. 2023, 24(17), 13236; https://doi.org/10.3390/ijms241713236 - 26 Aug 2023
Viewed by 1156
Abstract
Lower back pain, a leading cause of disability worldwide, is associated with intervertebral disc degeneration (IDD) in approximately 40% of cases. Although nucleus pulposus (NP) cell senescence is a major contributor to IDD, the underlying mechanisms remain unclear. We collected NP samples from [...] Read more.
Lower back pain, a leading cause of disability worldwide, is associated with intervertebral disc degeneration (IDD) in approximately 40% of cases. Although nucleus pulposus (NP) cell senescence is a major contributor to IDD, the underlying mechanisms remain unclear. We collected NP samples from IDD patients who had undergone spinal surgery. Healthy and senescent NP tissues (n = 3) were screened using the Pfirrmann grading system combined with immunohistochemistry, as well as hematoxylin and eosin, Safranin O, Alcian blue, and Masson staining. Differentially expressed proteins (DEPs) were identified using quantitative TMT-based proteomics technology. Bioinformatics analyses included gene ontology (GO) annotation, Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis, and protein–protein interaction (PPI) analyses. In addition, immunofluorescence was used to verify protein expression. In total, 301 DEPs were identified in senescent NP tissues, including 92 upregulated and 209 downregulated proteins. In GO, DEPs were primarily associated with NF-kappaB transcription factor, extracellular regions, cellular protein metabolic processes, and post-translational protein modification. The enriched KEGG pathways included TGF-β, Wnt, RAP1, interleukin-17, extracellular matrix-receptor adhesion, and PI3K/Akt signaling pathways. PPI analysis demonstrated interactions between multiple proteins. Finally, immunofluorescence verified the expressions of MMP3, LUM, TIMP1, and CDC42 in senescent NP cells. Our study provides valuable insights into the mechanisms underlying senescent NP tissues in IDD patients. DEPs provide a basis for further investigation of the effects of senescent factors on IDD. Full article
(This article belongs to the Special Issue Molecular Pathogenesis of Intervertebral Disc Disease)
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