“Cellular internet” circuitry is a process whereby donor cells communicate with recipient cells via extracellular signals, which reprograms the recipient cell behavior. This communication can be achieved by the direct cell-to-cell contacts, soluble ligand-receptor interactions, exosomes, apoptotic bodies/other extracellular vesicles, cytokines/chemokines, lipids, and hormones. Diverse cellular response is triggered by extracellular signals via specific receptor interactions followed by induction of signal transduction that leads to activation or death of these cells. In the context of alcohol exposure and/or high caloric consumption, the crosstalk within the liver between parenchymal and non-parenchymal cells modifies activation of the signal transduction pathway(s) and thus, the function of the recipient cells, causing the development of inflammation and fibrosis, with progression to end-stage liver disease. Similar “exchange” between various types of liver cells can occur by the release of viruses or viral proteins from virus-replicating cells or due to virus-triggered production of soluble receptors and cytokines/chemokines, which can further program the activation of neighboring liver cells and attract systemic pro-inflammatory cells. Importantly, these extracellular signals emanate not only from liver as an organ with high metabolizing capacity but can also come from other organs such as gut, adipose tissue, brain that also are affected by alcohol, high-caloric intake and/or viral infections.
For this Research Topic, we encourage the submission of original or review articles covering the role of cell-to-cell interactions in liver injury pathogenesis, outcomes and treatments in the settings of alcohol-associated liver disease, metabolic-related fatty liver disease and viral hepatitis.
“Cellular internet” circuitry is a process whereby donor cells communicate with recipient cells via extracellular signals, which reprograms the recipient cell behavior. This communication can be achieved by the direct cell-to-cell contacts, soluble ligand-receptor interactions, exosomes, apoptotic bodies/other extracellular vesicles, cytokines/chemokines, lipids, and hormones. Diverse cellular response is triggered by extracellular signals via specific receptor interactions followed by induction of signal transduction that leads to activation or death of these cells. In the context of alcohol exposure and/or high caloric consumption, the crosstalk within the liver between parenchymal and non-parenchymal cells modifies activation of the signal transduction pathway(s) and thus, the function of the recipient cells, causing the development of inflammation and fibrosis, with progression to end-stage liver disease. Similar “exchange” between various types of liver cells can occur by the release of viruses or viral proteins from virus-replicating cells or due to virus-triggered production of soluble receptors and cytokines/chemokines, which can further program the activation of neighboring liver cells and attract systemic pro-inflammatory cells. Importantly, these extracellular signals emanate not only from liver as an organ with high metabolizing capacity but can also come from other organs such as gut, adipose tissue, brain that also are affected by alcohol, high-caloric intake and/or viral infections.
For this Research Topic, we encourage the submission of original or review articles covering the role of cell-to-cell interactions in liver injury pathogenesis, outcomes and treatments in the settings of alcohol-associated liver disease, metabolic-related fatty liver disease and viral hepatitis.
