作者: SF Bennaser , NC Bird
DOI: 10.7707/HMJ.V6I2.200
关键词: Transdifferentiation 、 Cell biology 、 Liver cytology 、 Lipid droplet 、 Pathology 、 Biology 、 Hepatic stellate cell 、 Glial fibrillary acidic protein 、 Liver injury 、 Desmin 、 Cytoplasm
摘要: Quiescent hepatic stellate cells (HSCs) are characterized by their localization of perisinusoidal and long cytoplasmic processes, extending both along around the sinusoids as well between hepatocytes. These which have numerous vitamin A-containing lipid droplets, essential for identification HSCs in quiescent phase. Glial fibrillary acidic protein (GFAP) (Abcam, Cambridge, UK) is another crucial marker may allow a distinction to be made other fibroblastic liver cells. However, induction alpha-smooth muscle actin (α-SMA) most reliable cell activation because it absent from resident hepatocytes normal or injured liver, with exception smooth surrounding large vessels where present. Desmin has been used typical contractile rodent livers; however, its expression unreliable humans. Furthermore, HSCs’ transdifferentiation active phase proven rely on E-cadherin switching N-cadherin during HSC activation. Significant evidence now exists consider main matrix-producing process fibrosis. Liver injury, regardless aetiology, tumour growth metastases will ultimately lead HSCs. Several studies dissected molecular mechanisms involved fibrosis, intimately connected As result, number key steps fibrogenesis identified potential therapeutic targets that clinically useful preventing, treating,