Standardised Forms of Chondroitin Sulfate as a Pathogenetic Treatment of Osteoarthritis in the Context of Post-Genomic Studies
A systematic analysis of 37 post-genomic osteoarthritis (OA) studies (genomics, transcriptomics, proteomics, metabolomics) allowed to isolate 483 genes and corresponding proteins, their levels and activity disturbances are involved in the pathogenesis of the disease. These proteins can be conditiona...
| Main Authors: | , , , , |
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| Format: | Article |
| Language: | Russian |
| Published: |
IMA-PRESS LLC
2021-02-01
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| Series: | Современная ревматология |
| Subjects: | |
| Online Access: | https://mrj.ima-press.net/mrj/article/view/1112 |
| Summary: | A systematic analysis of 37 post-genomic osteoarthritis (OA) studies (genomics, transcriptomics, proteomics, metabolomics) allowed to isolate 483 genes and corresponding proteins, their levels and activity disturbances are involved in the pathogenesis of the disease. These proteins can be conditionally subdivided into three groups: 1) structural proteins of connective tissue (CT); 2) proteins that support the activity of CT growth factors; 3) proteins that promote CT remodeling and degradation, as well as proteins associated with the regulation of inflammation (cellular response to tumor necrosis factor α, interleukin 1, bacterial lipopolysaccharides, NF-κB activation, etc.). It is important to note the epigenetic effects (DNA hypomethylation) associated with the pathogenesis of OA, which indicates the need for the use of vitamins group B in the therapy. Chondroprotectors (symptomatic slow-acting drugs) – chondroitin sulfate (CS) and glucosamine sulfate (GS), – in addition to reducing inflammation through inhibition of NF-κB and lipopolysaccharide receptors (Toll-receptors), also contribute to an increase in the expression of genes for structural CT proteins, CT growth factors and modulate the activity of CT remodeling and degradation proteins. These effects of CS/GS allowed to describe the complex mechanisms of the pathogenetic action of CS/GS in the treatment of OA. |
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| ISSN: | 1996-7012 2310-158X |