About this Research Topic
Fibrosis is a leading cause of morbidity and mortality worldwide. The United States government estimates that 45% of death in USA can be attributed to fibrotic disorders. Liver fibrosis and its end stage, liver cirrhosis, is the final common pathway of chronic liver diseases. Patients with liver cirrhosis are facing tremendous risk of hepatic failure. Furthermore, more than 80% hepatocellular carcinoma patients derive from liver cirrhosis.
Advancement of liver fibrosis is a dynamic process characterised by accumulation exceeding degradation of extracellular matrix (ECM). Over the last two decades, sinusoidal resident hepatic stellate cells (HSCs) have been commonly recognised as the major source of ECM. HSC activation and transdifferentiation into myofibroblasts (MFBs) are key events in liver fibrogenesis. The initiation phase of HSC activation is due to paracrine stimuli from injured neighboring cells, including hepatocytes, Kupffer cells, sinusoidal endothelial cells, platelets and infiltrating inflammatory cells. These damaged cells secret a number of cytokines, chemokines and growth factors to activate HSCs. The important pro-fibrotic factors among them include transforming growth factor (TGF)-, connective tissue growth factor (CTGF), platelet-derived growth factor (PDGF), Interleukins, et al.
We plan to welcome active experts in this field to review the advancement on the role of the pro-fibrotic factors in liver fibrosis. The Research Topic will focus on the signaling of these important pro-fibrotic factors in HSCs during liver fibrogenesis.
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