| Autor: |
Bharti, Sneha, Agnihotri, Prachi, Biswas, Sagarika |
| Předmět: |
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| Zdroj: |
Trends in Carbohydrate Research; 2020, Vol. 12 Issue 2, p17-25, 9p |
| Abstrakt: |
Osteoarthritis (OA) is a joint disease associated with the disability and deformation of the cartilage. The damage in cartilage is due to the alteration in the structure and function of the proteins via different post-translational modifications. Phosphorylation of proteins and glycoproteins is found to be the important modification which deviates the normal condition of the cartilage that causes OA. Recent studies have revealed the effect of glycosylation, particularly GlcNAcylation, on the rate of the phosphorylation process and in turn their after-effects. The osteopontin, STAT3, MMP13, p53 and SMAD3 proteins are associated with the progression of OA as their phosphorylation/dephosphorylation causes inflammation through different cytokine pathways. Phosphoglycosylated proteins, YKL-39 and YKL-40 are some of the glycoproteins which are involved in OA pathogenesis. They are associated with MAPK and TLR4/MyD88-mediated JNK pathway to increase inflammation. Osteopontin suppresses the cartilage reactions via the ERK1/2 signaling pathway. STAT3 promotes expression of MMP13 via IL-6/STAT3 pathway. MMP13 mainly involves in ECM and cartilage degradation. The p53 upregulation leads to chondrocytes degradation and SMAD3 mutation could result in aneurysm-osteoarthritis syndrome. In downstream signaling cascade, targets of these phosphorylated proteins trigger the pro-inflammatory cytokine pathways, such as IL-6 and TNF-a which causes deformation of the cartilage and show significant responses to control over the severity of OA condition. This review enables us to know about the impact of phosphorylation/dephosphorylation of proteins, glycoproteins and their associated pathways involved in OA progression. These proteins could be therapeutic targets to control the disease condition. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
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