Non-alcoholic fatty liver disease (NAFLD) is estimated to affect 30% of the population and is one of the leading causes of abnormal liver function. NAFLD is highly associated with obesity and insulin resistance as over 70% of patients with type 2 diabetes have this disease. NAFLD covers a wide spectrum of liver pathology ranging from fatty liver to non-alcoholic steatohepatitis (NASH), which is characterized by steatosis, inflammation, hepatocellular injury, and fibrosis. Notably, immune cell-driven inflammation is a significant mechanism in the transition from fatty liver to the more serious NASH. Crosstalk between immune cells in metabolic tissues dictates the overall inflammatory tone and systemic metabolic homeostasis. Recent evidence indicates that immunological imbalances in the liver support the maintenance and progression of inflammation in NASH. Hepatic inflammation, driven by liver-resident immune cells, is a critical component in the initiation and progression of NASH. In general, NASH is characterized by a robust recruitment of immune cells into the liver where they become activated and have the capacity to release molecules that cause inflammation. While a dysregulated immune response can lead to disease, the inflammatory response early during liver injury may also be important for healing and tissue repair. While many therapeutic options are available to treat the metabolic derangements that coexist with the disease, there is currently no approved pharmacologic treatments for NAFLD itself.
This Research Topic aims to assemble the latest evidence describing immune mechanisms of NASH with a focus on the innate and adaptive immune pathways that become activated during disease. We welcome the submission of Original Research, Review, and Mini Review articles including, but not limited to, the following subtopics:
- Innate and Adaptive effector mechanisms in NASH
- Triggers of inflammation in NASH
- Inflammation-driven hepatocellular carcinoma (HCC)
- Crosstalk between liver and other organs in the triggering of NASH
- Lipotoxic hepatocellular stress
Non-alcoholic fatty liver disease (NAFLD) is estimated to affect 30% of the population and is one of the leading causes of abnormal liver function. NAFLD is highly associated with obesity and insulin resistance as over 70% of patients with type 2 diabetes have this disease. NAFLD covers a wide spectrum of liver pathology ranging from fatty liver to non-alcoholic steatohepatitis (NASH), which is characterized by steatosis, inflammation, hepatocellular injury, and fibrosis. Notably, immune cell-driven inflammation is a significant mechanism in the transition from fatty liver to the more serious NASH. Crosstalk between immune cells in metabolic tissues dictates the overall inflammatory tone and systemic metabolic homeostasis. Recent evidence indicates that immunological imbalances in the liver support the maintenance and progression of inflammation in NASH. Hepatic inflammation, driven by liver-resident immune cells, is a critical component in the initiation and progression of NASH. In general, NASH is characterized by a robust recruitment of immune cells into the liver where they become activated and have the capacity to release molecules that cause inflammation. While a dysregulated immune response can lead to disease, the inflammatory response early during liver injury may also be important for healing and tissue repair. While many therapeutic options are available to treat the metabolic derangements that coexist with the disease, there is currently no approved pharmacologic treatments for NAFLD itself.
This Research Topic aims to assemble the latest evidence describing immune mechanisms of NASH with a focus on the innate and adaptive immune pathways that become activated during disease. We welcome the submission of Original Research, Review, and Mini Review articles including, but not limited to, the following subtopics:
- Innate and Adaptive effector mechanisms in NASH
- Triggers of inflammation in NASH
- Inflammation-driven hepatocellular carcinoma (HCC)
- Crosstalk between liver and other organs in the triggering of NASH
- Lipotoxic hepatocellular stress
