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Advanced glycation end products promote VEGF expression and thus choroidal
neovascularization via Cyr61-PI3K/AKT signaling pathway
#MMPMID29097668
Sun L
; Huang T
; Xu W
; Sun J
; Lv Y
; Wang Y
Sci Rep
2017[Nov]; 7
(1
): 14925
PMID29097668
show ga
Choroidal neovascularisation (CNV) causes severe vision loss among old patients,
especially those with diabetes. Previously, Cyr61 has been found to play a
critical role in the pathogenesis of both AMD and diabetes. In the present study,
we found that increased CNV severity together with higher expression of Cyr61 and
VEGF in diabetes mice compared with control mice. Moreover, knockdown of Cyr61
decreased CNV severity. In vitro mechanism study revealed that the advanced
glycation end products (AGEs) significantly increased the expression of Cyr61 in
retinal pigment epithelial (RPE) cells, mimicking the effects of diabetes. In
turn, the increased Cyr61 enhanced VEGF expression through FAK and PI3K/Akt
pathways. Chemically blocking the above pathway significantly inhibited CNV
formation, providing a new strategy for clinical prevention and treatment of CNV
in related diseases.
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