α7KO mice fed an AD showed significant upregulation of the Col1a1 gene encoding alpha-1 type I collagen, which is involved in liver fibrosis, and the Ccl2 gene encoding C-C motif chemokine ligand 2, a pro-inflammatory chemokine; α7KO mice fed an MCD had significant upregulation of the Col1a1 gene and the Tnf gene, an inflammatory cytokine.
With the severity of liver fibrosis, the expression of TGF-β, α-SMA, Smad3 and CTGF gradually increased, and the difference was statistically significant (p < 0.01).
With the severity of liver fibrosis, the expression of TGF-β, α-SMA, Smad3 and CTGF gradually increased, and the difference was statistically significant (p < 0.01).
With further validation, plasma DNA methylation of PPARγ could potentially be used to non-invasively stratify liver fibrosis severity in patients with NAFLD.
Wisteria floribunda agglutinin-positive human Mac-2 binding protein (WFA<sup>+</sup> -M2BP) can be used to assess the degree of liver fibrosis, but few studies have investigated its prognostic utility.
Wisteria floribunda agglutinin-positive Mac-2-binding protein (WFA<sup>+</sup> -M2BP) is a novel glycobiomarker for evaluating liver fibrosis, but less is known about its role in liver cirrhosis (LC).
Wisteria floribunda agglutinin-positive Mac-2 binding protein (WFA<sup>+</sup> -M2BP) is a novel serum marker of hepatic fibrosis in adults with chronic hepatitis C. However, it remains unclear whether serum WFA<sup>+</sup> -M2BP levels are associated with the progression of liver histology in primary sclerosing cholangitis (PSC).
While vascular RAGE expression is associated with kidney and liver fibrosis, high expression levels of RAGE are found under physiological conditions in the lung.
While the PI3K/mTOR pathway appears to be a promising target for the treatment of liver fibrosis, PCTS revealed likely side effects in the intestine at higher doses.
While the PI3K/mTOR pathway appears to be a promising target for the treatment of liver fibrosis, PCTS revealed likely side effects in the intestine at higher doses.
While the PI3K/mTOR pathway appears to be a promising target for the treatment of liver fibrosis, PCTS revealed likely side effects in the intestine at higher doses.
While the PI3K/mTOR pathway appears to be a promising target for the treatment of liver fibrosis, PCTS revealed likely side effects in the intestine at higher doses.
While studies in animal models have linked Toll-like receptor (TLR) 4 signaling to the pathophysiology of ischemia/reperfusion (IR) injury and liver fibrosis, the relevance of TLR4 activation after human liver transplantation is unknown.
While different signaling pathways are involved in liver fibrosis progression, mitogen-activated protein kinase (MAPK) and phosphoinositide-3-kinase-protein kinase B/Akt (PI3K/Akt) are the most crucial.
While different signaling pathways are involved in liver fibrosis progression, mitogen-activated protein kinase (MAPK) and phosphoinositide-3-kinase-protein kinase B/Akt (PI3K/Akt) are the most crucial.
While different signaling pathways are involved in liver fibrosis progression, mitogen-activated protein kinase (MAPK) and phosphoinositide-3-kinase-protein kinase B/Akt (PI3K/Akt) are the most crucial.
While different signaling pathways are involved in liver fibrosis progression, mitogen-activated protein kinase (MAPK) and phosphoinositide-3-kinase-protein kinase B/Akt (PI3K/Akt) are the most crucial.
Whereas hepatic levels of CTGF/CCN2 are usually low, elevated levels of hepatic CTGF/CCN2 occur in patients with liver fibrosis and in experimental animal models of liver fibrosis.
When we depleted the Vγ2 T cells in infected mice, the percentage of neutrophils in blood and spleen decreased significantly, the liver fibrosis in the granulomas was reduced, and the level of IL-17A in the serum decreased (<i>P</i> < 0.05).These results suggest that during <i>S. japonicum</i> infection, Vγ2 T cells can recruit neutrophils and aggravate liver fibrosis by secreting IL-17A.