Assessment of renal fibrosis in a rat model of unilateral ureteral obstruction with diffusion kurtosis imaging: Comparison with α-SMA expression and <sup>18</sup>F-FDG PET.
Overexpression of YY1 promoted renal fibrosis in db/m mice mainly by upregulating α-SMA expression and inducing epithelial-mesenchymal transition (EMT) in vitro and in vivo.
In vitro studies revealed that overexpression of cytoglobin suppressed phosphorylation of Smad2, ERK, and p38 induced by TGF-β and expression of NF-kB, α-SMA, and TGF-β RI.LDP prevented renal fibrosis and protected glomerular mesangial cells by upregulation of cytoglobin and suppression of multiple pathways involving TGF-β/SMADS, MAPK, NF-kB signaling.
In vivo, PFD reduced the degree of tubulointerstitial injury and renal fibrosis, which was associated with reduced expression of TGF-β1, type III collagen, α-SMA, S100A4, fibronection, and increased expression of E-cadherin.
The activation of interstitial fibroblasts to become alpha-SMA-positive myofibroblasts is an essential step in the evolution of chronic kidney fibrosis, as myofibroblasts are responsible for the production and deposition of the ECM components that are a hallmark of the disease.