Obesity is a major type of chronic disease that has reached an epidemic proportion worldwide. It is closely associated with a spectrum of liver abnormalities, now coined as metabolic associated fatty liver disease (MAFLD). MAFLD is characterized by an increase in intrahepatic triglycerides (steatosis), in parallel with marked inflammation (steatohepatitis) with or without fibrosis, and affects nearly one billion people globally. However, there is currently no approved drug therapy for the disease, predominantly due to the lack of versatile therapeutic targets. In addition, liver biopsy remains the current gold standard for the diagnosis and staging of MAFLD, due to the lack of known non-invasive biomarkers.
Pathological events, such as chronic inflammation, endoplasmic reticulum (ER) stress, cellular senescence, insulin resistance, aberrant lipid metabolism, oxidative stress, and mitochondrial dysfunction, have all been implicated in the development and progression of the disease. The pathology is further complicated by the fact that the crosstalk between liver and other organs, including adipose tissue, skeletal muscle, gut and liver microbiome, also plays a pivotal role in MAFLD pathology. Nevertheless, the detailed mechanisms by which endocrine factors are involved are still not completely understood. A better understanding of the pathogenic mechanisms involved in MAFLD is of great importance to establish more precise and non-invasive diagnostic methods, and to inspire novel approaches for management as well as prevention of MAFLD.
This Research Topic will focus on how insights into the molecular mechanisms underlying MAFLD, are improving our knowledge of diagnostic biomarkers and therapeutic interventions of the disease.
We will accept both review and research articles on either animal and human studies, covering the cellular and molecular mechanisms, as well as new strategies for diagnosis, prevention and treatment of MAFLD, especially in the following aspects:
• Key mechanisms by which ER stress and cellular senescence are involved in MAFLD pathology
• How the endocrine crosstalk between major organs (such as adipose tissue, muscle, gut, etc.) and the liver, contributes to MAFLD
• Biomarkers for risk prediction and diagnosis of MAFLD
• Clinical studies in to molecular targets and intervention for management of MAFLD
Obesity is a major type of chronic disease that has reached an epidemic proportion worldwide. It is closely associated with a spectrum of liver abnormalities, now coined as metabolic associated fatty liver disease (MAFLD). MAFLD is characterized by an increase in intrahepatic triglycerides (steatosis), in parallel with marked inflammation (steatohepatitis) with or without fibrosis, and affects nearly one billion people globally. However, there is currently no approved drug therapy for the disease, predominantly due to the lack of versatile therapeutic targets. In addition, liver biopsy remains the current gold standard for the diagnosis and staging of MAFLD, due to the lack of known non-invasive biomarkers.
Pathological events, such as chronic inflammation, endoplasmic reticulum (ER) stress, cellular senescence, insulin resistance, aberrant lipid metabolism, oxidative stress, and mitochondrial dysfunction, have all been implicated in the development and progression of the disease. The pathology is further complicated by the fact that the crosstalk between liver and other organs, including adipose tissue, skeletal muscle, gut and liver microbiome, also plays a pivotal role in MAFLD pathology. Nevertheless, the detailed mechanisms by which endocrine factors are involved are still not completely understood. A better understanding of the pathogenic mechanisms involved in MAFLD is of great importance to establish more precise and non-invasive diagnostic methods, and to inspire novel approaches for management as well as prevention of MAFLD.
This Research Topic will focus on how insights into the molecular mechanisms underlying MAFLD, are improving our knowledge of diagnostic biomarkers and therapeutic interventions of the disease.
We will accept both review and research articles on either animal and human studies, covering the cellular and molecular mechanisms, as well as new strategies for diagnosis, prevention and treatment of MAFLD, especially in the following aspects:
• Key mechanisms by which ER stress and cellular senescence are involved in MAFLD pathology
• How the endocrine crosstalk between major organs (such as adipose tissue, muscle, gut, etc.) and the liver, contributes to MAFLD
• Biomarkers for risk prediction and diagnosis of MAFLD
• Clinical studies in to molecular targets and intervention for management of MAFLD
