Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28097825
&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests
in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215
Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534
Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534
Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\28097825
.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 J+Cell+Mol+Med
2017 ; 21
(7
): 1248-1259
Nephropedia Template TP
gab.com Text
Twit Text FOAVip
Twit Text #
English Wikipedia
Signalling pathways involved in hypoxia-induced renal fibrosis
#MMPMID28097825
Liu M
; Ning X
; Li R
; Yang Z
; Yang X
; Sun S
; Qian Q
J Cell Mol Med
2017[Jul]; 21
(7
): 1248-1259
PMID28097825
show ga
Renal fibrosis is the common pathological hallmark of progressive chronic kidney
disease (CKD) with diverse aetiologies. Recent researches have highlighted the
critical role of hypoxia during the development of renal fibrosis as a final
common pathway in end-stage kidney disease (ESKD), which joints the scientist's
attention recently to exploit the molecular mechanism underlying hypoxia-induced
renal fibrogenesis. The scaring formation is a multilayered cellular response and
involves the regulation of multiple hypoxia-inducible signalling pathways and
complex interactive networks. Therefore, this review will focus on the signalling
pathways involved in hypoxia-induced pathogenesis of interstitial fibrosis,
including pathways mediated by HIF, TGF-?, Notch, PKC/ERK, PI3K/Akt, NF-?B, Ang
II/ROS and microRNAs. Roles of molecules such as IL-6, IL-18, KIM-1 and ADO are
also reviewed. A comprehensive understanding of the roles that these
hypoxia-responsive signalling pathways and molecules play in the context of renal
fibrosis will provide a foundation towards revealing the underlying mechanisms of
progression of CKD and identifying novel therapeutic targets. In the future,
promising new effective therapy against hypoxic effects may be successfully
translated into the clinic to alleviate renal fibrosis and inhibit the
progression of CKD.