Acute liver injury is a rather rare but often fatal condition. While the mechanisms leading to liver injury for certain etiologies (drug induced liver injury, acetaminophen poisoning) have been elucidated in detail, it remains unclear, what causes a fatal course in many types of liver damage. Similarly, little is known about the mechanisms that account for the diversity of clinical outcomes in acute liver failure, which range from spontaneous recovery to death or the need for orthotopic liver transplantation. Contribution of different hepatocyte cell death mechanisms, immune-competent cell populations, other non-parenchymal cell types and the metabolic status influence the regeneratory capacity of the damaged liver. Thus, wound healing processes including endothelial to mesenchymal transdifferentiation are in the focus of translational studies. New approaches for the treatment of certain etiologies and of acute liver failure in general could be derived from molecular targets or mechanisms involved in these processes. In addition, improved prognosis of patient outcome or accelerated identification of the underlying etiology may be facilitated by more detailed knowledge of effectors and targets related to acute liver failure. With this special topic edition, expert researchers working on the frontiers of hepatology will be asked to share their most current insights on the pathogenesis, underlying mechanisms, prediction of clinical outcome and therapeutic management of acute liver injury. Expert reviews should include state-of-the-art aspects of liver replacement therapy, hepatocyte transplantation, endothelial-to-mesenchymal transdifferentiation and metabolic pathways involved in liver regeneration. Reviewers are encouraged to discuss translational research, including cell culture data, in vivo models of acute liver injury and liver regeneration as well as clinical data.
Acute liver injury is a rather rare but often fatal condition. While the mechanisms leading to liver injury for certain etiologies (drug induced liver injury, acetaminophen poisoning) have been elucidated in detail, it remains unclear, what causes a fatal course in many types of liver damage. Similarly, little is known about the mechanisms that account for the diversity of clinical outcomes in acute liver failure, which range from spontaneous recovery to death or the need for orthotopic liver transplantation. Contribution of different hepatocyte cell death mechanisms, immune-competent cell populations, other non-parenchymal cell types and the metabolic status influence the regeneratory capacity of the damaged liver. Thus, wound healing processes including endothelial to mesenchymal transdifferentiation are in the focus of translational studies. New approaches for the treatment of certain etiologies and of acute liver failure in general could be derived from molecular targets or mechanisms involved in these processes. In addition, improved prognosis of patient outcome or accelerated identification of the underlying etiology may be facilitated by more detailed knowledge of effectors and targets related to acute liver failure. With this special topic edition, expert researchers working on the frontiers of hepatology will be asked to share their most current insights on the pathogenesis, underlying mechanisms, prediction of clinical outcome and therapeutic management of acute liver injury. Expert reviews should include state-of-the-art aspects of liver replacement therapy, hepatocyte transplantation, endothelial-to-mesenchymal transdifferentiation and metabolic pathways involved in liver regeneration. Reviewers are encouraged to discuss translational research, including cell culture data, in vivo models of acute liver injury and liver regeneration as well as clinical data.