Following the success of
Cross-Talk between Cellular and Molecular Compartments during Liver Injury we are pleased to present Volume II of this collection.
The unique structure and function of the liver result in the constant exposure to a series of stimuli, such as alcohol, high-fat diet, the influx of microbiota from gut and pathogens.
Liver injury, irrespective of etiology, involves persistent inflammatory response, parenchymal injury, and liver fibrogenesis. The progression of liver injury is a dynamic process that involves the multidirectional cross-talk between different cellular and molecular compartments. For example, macrophages can activate hepatic stellate cells (HSCs) into scar-forming myofibroblasts via TGF-ß, PDGF, galectin-3, and TNF-a, leading to liver fibrosis progression. Hepatocyte/cholangiocytes-macrophage-HSCs cross-talk increases the expression of pro-inflammatory cytokines to progress the liver injuries. The differentiation of hepatic stem cells is dependent on inflammatory cytokines, growth factors, and extracellular matrix secreted by cholangiocytes, HSCs, and macrophages. Nevertheless, the distinct cross-talk between cellular and molecular compartments in liver injury induced by specific etiology is very complex and remains largely unknown.
This Research Topic welcomes Original Research articles and Review submissions that cover emerging and new insights into how cells, various molecules, signaling pathways, and their cross-talk effect and induce liver injuries. New concepts and current mechanistic insights as well as future perspectives of detection, treatment, and prevention of the conditions in this field will be discussed.
Following the success of
Cross-Talk between Cellular and Molecular Compartments during Liver Injury we are pleased to present Volume II of this collection.
The unique structure and function of the liver result in the constant exposure to a series of stimuli, such as alcohol, high-fat diet, the influx of microbiota from gut and pathogens.
Liver injury, irrespective of etiology, involves persistent inflammatory response, parenchymal injury, and liver fibrogenesis. The progression of liver injury is a dynamic process that involves the multidirectional cross-talk between different cellular and molecular compartments. For example, macrophages can activate hepatic stellate cells (HSCs) into scar-forming myofibroblasts via TGF-ß, PDGF, galectin-3, and TNF-a, leading to liver fibrosis progression. Hepatocyte/cholangiocytes-macrophage-HSCs cross-talk increases the expression of pro-inflammatory cytokines to progress the liver injuries. The differentiation of hepatic stem cells is dependent on inflammatory cytokines, growth factors, and extracellular matrix secreted by cholangiocytes, HSCs, and macrophages. Nevertheless, the distinct cross-talk between cellular and molecular compartments in liver injury induced by specific etiology is very complex and remains largely unknown.
This Research Topic welcomes Original Research articles and Review submissions that cover emerging and new insights into how cells, various molecules, signaling pathways, and their cross-talk effect and induce liver injuries. New concepts and current mechanistic insights as well as future perspectives of detection, treatment, and prevention of the conditions in this field will be discussed.
