Acute liver injury seriously threatens human health, and can evolve to a lethal outcome within days or weeks. Causes of acute liver injury include liver ischemia–reperfusion injury (LIRI), viral hepatitis (e.g., hepatitis B virus (HBV) infection) and exposure to hepatotoxins. LIRI, one of the primary causes of early organ failure after liver transplantation, is a local sterile inflammatory response driven by innate immunity. Cellular damage resulting from LIRI is an important risk factor not only for graft malfunction but also for acute and chronic rejections, worsening the scarcity of donor organs. Currently, there is no effective treatment for acute liver failure. New insights into acute liver injury and therapeutic strategies are therefore greatly needed.
The goal of this research topic is to discuss the pathogenesis of acute liver injury and to develop effective therapeutic strategies. More specifically, we aim to explore the roles of cell death, immune response, and specific molecules in the pathogenesis of acute liver damage, such as LIRI, drug-induced liver injury, and acute alcoholic liver injury. Mechanisms underlying the acute liver injury and the resolving signaling pathways that tend to restrain the accelerating immune response to achieve homeostatic tissue repair remains unclear. Hence, this Research Topic focuses on the cellular and molecular mechanisms of acute liver injury and repair. We hope that this topic will provide cutting-edge insights into the function of pro- and anti-inflammatory responses in acute liver injury, as well as a foundation for investigating new acute liver injury therapies.
This research topic will cover research articles, (mini)reviews, hypotheses, commentaries, and perspectives in this field. Potential topics include but are not limited to the following:
• Novel cellular and molecular mechanisms of liver ischemia-reperfusion injury and related diseases.
• Cellular and molecular mechanisms of drug-induced liver injury and other liver diseases.
• Cellular and molecular mechanisms of liver regeneration and repair.
• New Insights into cell differentiation and cell death including ferroptosis, necroptosis, autophagy, apoptosis, and pyroptosis in the process of acute liver injury, regeneration, repair, and fibrosis.
Acute liver injury seriously threatens human health, and can evolve to a lethal outcome within days or weeks. Causes of acute liver injury include liver ischemia–reperfusion injury (LIRI), viral hepatitis (e.g., hepatitis B virus (HBV) infection) and exposure to hepatotoxins. LIRI, one of the primary causes of early organ failure after liver transplantation, is a local sterile inflammatory response driven by innate immunity. Cellular damage resulting from LIRI is an important risk factor not only for graft malfunction but also for acute and chronic rejections, worsening the scarcity of donor organs. Currently, there is no effective treatment for acute liver failure. New insights into acute liver injury and therapeutic strategies are therefore greatly needed.
The goal of this research topic is to discuss the pathogenesis of acute liver injury and to develop effective therapeutic strategies. More specifically, we aim to explore the roles of cell death, immune response, and specific molecules in the pathogenesis of acute liver damage, such as LIRI, drug-induced liver injury, and acute alcoholic liver injury. Mechanisms underlying the acute liver injury and the resolving signaling pathways that tend to restrain the accelerating immune response to achieve homeostatic tissue repair remains unclear. Hence, this Research Topic focuses on the cellular and molecular mechanisms of acute liver injury and repair. We hope that this topic will provide cutting-edge insights into the function of pro- and anti-inflammatory responses in acute liver injury, as well as a foundation for investigating new acute liver injury therapies.
This research topic will cover research articles, (mini)reviews, hypotheses, commentaries, and perspectives in this field. Potential topics include but are not limited to the following:
• Novel cellular and molecular mechanisms of liver ischemia-reperfusion injury and related diseases.
• Cellular and molecular mechanisms of drug-induced liver injury and other liver diseases.
• Cellular and molecular mechanisms of liver regeneration and repair.
• New Insights into cell differentiation and cell death including ferroptosis, necroptosis, autophagy, apoptosis, and pyroptosis in the process of acute liver injury, regeneration, repair, and fibrosis.
