Direct contribution of epithelium to organ fibrosis: epithelial-mesenchymal transition

Involvement of matrix metalloproteinase-2 in the development of renal interstitial fibrosis in mouse obstructive nephropathy

“…[1][2][3][4][5][6][7][8][9][10][11][12] Damaged tubular epithelial cells have mesenchymal phenotype through EMT, and migrate into interstitium. [7][8][9][10][11][12] Indeed, one recent study using a gGTLacZ transgenic mice, which allows the indisputable identification of cells derived from proximal tubular epithelium in the kidney, reported that more than one-third of renal interstitial fibroblasts were derived from renal tubular epithelium through EMT. 28 MMP-2 and MMP-9, which mediate TBM degradation, are considered a critical event in renal EMT.…”

“…[4][5][6] Recent studies have emphasized the potential role of epithelial-tomesenchymal transition (EMT) in the development of renal interstitial fibrosis. [7][8][9][10][11][12] Tubular epithelial cells can acquire a mesenchymal phenotype after several injuries, enhance migratory capacity enabling them to transit from the renal tubular microenvironment into the interstitial space, and contribute to the development of renal fibrosis as ECMproducing myofibroblasts. The role of EMT in renal fibrogenesis has been suggested in several studies of cultured cells, animal models of kidney diseases, and human nephropathies and kidney transplantation, [7][8][9][10][11][12] although several recent studies also demonstrate the doubt on this mechanism as a major contributor to renal fibrosis.…”

“…[7][8][9][10][11][12] Tubular epithelial cells can acquire a mesenchymal phenotype after several injuries, enhance migratory capacity enabling them to transit from the renal tubular microenvironment into the interstitial space, and contribute to the development of renal fibrosis as ECMproducing myofibroblasts. The role of EMT in renal fibrogenesis has been suggested in several studies of cultured cells, animal models of kidney diseases, and human nephropathies and kidney transplantation, [7][8][9][10][11][12] although several recent studies also demonstrate the doubt on this mechanism as a major contributor to renal fibrosis. [13][14][15] Matrix metalloproteinases (MMPs) are a family of zincdependent proteases responsible for ECM turnover as well as degradation of bioactive proteins.…”

Alterations of Wnt/β-catenin signaling pathway in hepatocellular carcinomas associated with hepatitis C virus

“…Disturbances in structure and function of ECCU were detected in the process of organ fibrosis, including liver fibrosis [49]. The process is closely linked to decreased expression of E-cadherin and overexpression of β-catenin with its cytoplasmic translocation, which results in a loss of intercellular junctions [45].…”

Effect of entecavir in the treatment of patients with hepatitis B virus-related compensated and decompensated cirrhosis

“…An epidemiological survey reported that 15-40% of HBV carriers are at a higher risk of serious sequelae, including cirrhosis and hepatocellular carcinoma (HCC) (3). Cirrhosis is the end stage of chronic liver damage, which is reflected by liver fibrosis and liver architecture destruction (4). HBV, Hepatitis C (HCV) and alcohol consumption are major contributors to the development of cirrhosis, of which HBV infection accounts for ~1/3 of cirrhosis cases globally (5).…”