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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.