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pmid26464640
      Int+J+Clin+Exp+Pathol 2015 ; 8 (8 ): 8983-9
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  • Knockdown of elF3a inhibits collagen synthesis in renal fibroblasts via Inhibition of transforming growth factor-?1/Smad signaling pathway #MMPMID26464640
  • Zhang YF ; Wang Q ; Luo J ; Yang S ; Wang JL ; Li HY
  • Int J Clin Exp Pathol 2015[]; 8 (8 ): 8983-9 PMID26464640 show ga
  • Renal fibrosis is characterized by an exacerbated accumulation of deposition of the extracellular matrix (ECM). The eukaryotic translation initiation factor (eIF) 3a is the largest subunit of the eIF3 complex and has been involved in pulmonary fibrosis. However, the role of eIF3a in rental fibrosis is still unclear. Therefore, in this study, we investigated the role of eIF3a in rental fibrosis and explored the underlying mechanism. Our study found that eIF3a was up-regulated in renal fibrotic tissues and transforming growth factor (TGF)-?1-treated HK-2 cells. In addition, knockdown of eIF3a significantly inhibited TGF-?1-induced expression levels of ?-smooth muscle actin (?-SMA) and collagen I. Furthermore, knockdown of eIF3a attenuated TGF-?1-induced Smad3 activation in HK-2 cells. Taken together, these results suggest that knockdown of eIF3a inhibits collagen synthesis in renal fibroblasts via inhibition of TGF-?1/Smad signaling pathway, and eIF3a may be a potential molecular target for the treatment of renal fibrosis.
  • |Cell Line [MESH]
  • |Collagen/*metabolism [MESH]
  • |Eukaryotic Initiation Factor-3/*genetics/metabolism [MESH]
  • |Fibroblasts/*metabolism/pathology [MESH]
  • |Fibrosis/genetics/metabolism/pathology [MESH]
  • |Humans [MESH]
  • |Kidney Diseases/genetics/*metabolism/pathology [MESH]
  • |Kidney/*metabolism/pathology [MESH]
  • |Phosphorylation [MESH]
  • |Signal Transduction/genetics [MESH]
  • |Smad Proteins/genetics/*metabolism [MESH]
  • |Transforming Growth Factor beta1/genetics/*metabolism [MESH]


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