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In most fibrotic disorders, CTGF acts as a downstream effector of TGF-β to promote the phenotypic conversion of fibroblastic cells to the myofibroblasts that conduct fibrosis (Ihn 2002; Dendooven et al. 2011).
Most fibrotic diseases also manifest substantial vascular remodeling with impaired angiogenesis followed by progressive obliteration of blood vessels that is often an early feature suggesting that endothelial injury may be a precipitating event in fibrosis pathogenesis [150-152].
Excessive deposition of extracellular matrix (ECM) molecules is characteristic of most fibrotic tissues.
In other words, the 95th percentile represents the most fibrotic areas within the ROI.
Subsequently, this same myofilament protein (αSMA) was demonstrated in most fibrotic processes in multiple tissues from various species [ 44, 45].
It is common consent that hepatic stellate cells (HSC) are the main source of collagen in most fibrotic liver diseases.
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Liver fibrosis is one of the most frequent fibrotic disorders affecting humans and has multiple and diverse causes including hepatitis virus infections and excessive ethanol consumption, frequently resulting in liver failure and portal hypertension [242].
Schistosomiasis mansoni is considered one of the most common fibrotic diseases resulting from inflammation and deposition of fibrous tissue around parasitic eggs trapped in the liver, causing morbidity and mortality.
TGFB, considered to be the most important fibrotic factor, has been shown to upregulate CTGF in many cell types in vitro [ 42– 44] and in vivo [ 45, 46].
TGF-β1 has been identified as the most pro-fibrotic cytokine, being responsible, for instance, for hepatic stellate cell trans-differentiation into myofibroblast in the first stages of liver fibrosis [ 6].
MCP caused significant attenuation of the increases for most of these fibrotic markers (α-SMA p<0.01; collagen I, fibronectin and TGFβ1 p<0.05); but again did not alter collagen III (p = 0.18).
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