Fatty liver disease, encompassing metabolic-associated fatty liver disease (MAFLD) and alcohol-associated liver disease (ALD), is now a significant global health issue. MAFLD is closely linked to metabolic syndrome, obesity, and type 2 diabetes, making it the leading cause of chronic liver disease. ALD results from excessive alcohol intake and leads to various liver conditions, including steatosis, steatohepatitis, fibrosis, and cirrhosis. Both MAFLD and ALD involve fat buildup in the liver (steatosis) and inflammation but differ in their causes and some pathogenic processes.
Recent studies emphasize the gut-liver axis, lipid metabolism issues, mitochondrial dysfunction, and oxidative stress in disease progression. Despite advancements in understanding these mechanisms, effective pharmacological treatments are scarce, and non-invasive diagnostic tools are urgently needed. This Research Topic aims to thoroughly explore these molecular mechanisms and novel treatment strategies for fatty liver disease.
MAFLD and ALD are now the top causes of chronic liver disease globally. Both conditions involve excessive liver fat accumulation, leading to inflammation, fibrosis, and, in severe cases, cirrhosis or hepatocellular carcinoma. While both share mechanisms like lipotoxicity, oxidative stress, and inflammation, distinct molecular triggers differentiate them. Despite increased awareness, the exact molecular mechanisms from simple steatosis to severe liver damage remain unclear. Moreover, effective treatments to stop or reverse disease progression are limited.
This Research Topic seeks to gather insights into the cellular and molecular mechanisms of MAFLD and ALD development and progression, including lipid metabolism, gut-liver axis dysfunction, genetic and epigenetic factors, and the interaction between alcohol and metabolic stressors. By exploring these areas, we aim to identify new molecular targets and treatments for better management of fatty liver disease.
In this Research Topic, we invite research articles and reviews on the cellular, molecular, and gut-liver axis mechanisms involved in the pathogenesis and progression of MAFLD, ALD, and related conditions. We encourage submissions on topics such as:
• Gut microbiota dysbiosis and its impact on liver diseases
• Intestinal permeability and endotoxin-related liver injury
• Lipid metabolism issues in steatohepatitis
• Immune responses in MAFLD and ALD
• Oxidative stress and mitochondrial dysfunction
• Epigenetic and genetic factors in disease progression
We look forward to your contributions to enhance our understanding of MAFLD and ALD and develop innovative treatments.
Fatty liver disease, encompassing metabolic-associated fatty liver disease (MAFLD) and alcohol-associated liver disease (ALD), is now a significant global health issue. MAFLD is closely linked to metabolic syndrome, obesity, and type 2 diabetes, making it the leading cause of chronic liver disease. ALD results from excessive alcohol intake and leads to various liver conditions, including steatosis, steatohepatitis, fibrosis, and cirrhosis. Both MAFLD and ALD involve fat buildup in the liver (steatosis) and inflammation but differ in their causes and some pathogenic processes.
Recent studies emphasize the gut-liver axis, lipid metabolism issues, mitochondrial dysfunction, and oxidative stress in disease progression. Despite advancements in understanding these mechanisms, effective pharmacological treatments are scarce, and non-invasive diagnostic tools are urgently needed. This Research Topic aims to thoroughly explore these molecular mechanisms and novel treatment strategies for fatty liver disease.
MAFLD and ALD are now the top causes of chronic liver disease globally. Both conditions involve excessive liver fat accumulation, leading to inflammation, fibrosis, and, in severe cases, cirrhosis or hepatocellular carcinoma. While both share mechanisms like lipotoxicity, oxidative stress, and inflammation, distinct molecular triggers differentiate them. Despite increased awareness, the exact molecular mechanisms from simple steatosis to severe liver damage remain unclear. Moreover, effective treatments to stop or reverse disease progression are limited.
This Research Topic seeks to gather insights into the cellular and molecular mechanisms of MAFLD and ALD development and progression, including lipid metabolism, gut-liver axis dysfunction, genetic and epigenetic factors, and the interaction between alcohol and metabolic stressors. By exploring these areas, we aim to identify new molecular targets and treatments for better management of fatty liver disease.
In this Research Topic, we invite research articles and reviews on the cellular, molecular, and gut-liver axis mechanisms involved in the pathogenesis and progression of MAFLD, ALD, and related conditions. We encourage submissions on topics such as:
• Gut microbiota dysbiosis and its impact on liver diseases
• Intestinal permeability and endotoxin-related liver injury
• Lipid metabolism issues in steatohepatitis
• Immune responses in MAFLD and ALD
• Oxidative stress and mitochondrial dysfunction
• Epigenetic and genetic factors in disease progression
We look forward to your contributions to enhance our understanding of MAFLD and ALD and develop innovative treatments.