In the past, the accumulation of lipids in the liver was considered a reflection of generalized adiposity. Follow-up studies on patients with liver steatosis have shown that in a substantial group of subjects, it may result in steatohepatitis and cirrhosis. With improvements in antiviral therapy, MASLD has become the most common chronic liver disease and is emerging as a major cause of liver transplantations. The development of MASLD is still not fully understood. Certainly, the obesity pandemic is an important contributor, but there are also lean patients with advanced MASLD. Other factors include insulin, adipokine signaling, incretin signaling, and gut microbiota. Further studies to explore additional contributing factors are necessary to halt the progression of the disease. Currently, there are few widely accepted therapeutic strategies to improve patients' outcomes. Available pharmacotherapy includes drugs that may accelerate weight loss (GLP-1 analogs), improve the course of diabetes or heart failure (SGLT-2 inhibitors), or taper inflammation in steatohepatitis (vitamin E, pioglitazone, GLP-1 analogs). Other approaches to deal with MASLD are currently under development (e.g., multiple incretin analogs, PPAR agonists).
Therefore, I invite authors to contribute papers, both in vitro and in vivo, depicting the search for novel pathophysiological pathways involved in the development of MASLD, potential preventive measures to reduce the burden of MASLD, and tentative therapeutic targets that might prove useful in the treatment of the disease. Comprehensive reviews that analyze the aforementioned subjects and include compelling areas for further research are also welcome.
Topics of interest include, but are not limited to:
• MASLD
• obesity
• cardiovascular risk factors
• incretins
• GLP-1
• SGLT-2
• vitamin E
• pharmacotherapy of MASLD
• pathophysiology of MASLD
• therapeutic lifestyle change
• steatosis
• steatohepatitis
• liver fibrosis
• liver cirrhosis
In the past, the accumulation of lipids in the liver was considered a reflection of generalized adiposity. Follow-up studies on patients with liver steatosis have shown that in a substantial group of subjects, it may result in steatohepatitis and cirrhosis. With improvements in antiviral therapy, MASLD has become the most common chronic liver disease and is emerging as a major cause of liver transplantations. The development of MASLD is still not fully understood. Certainly, the obesity pandemic is an important contributor, but there are also lean patients with advanced MASLD. Other factors include insulin, adipokine signaling, incretin signaling, and gut microbiota. Further studies to explore additional contributing factors are necessary to halt the progression of the disease. Currently, there are few widely accepted therapeutic strategies to improve patients' outcomes. Available pharmacotherapy includes drugs that may accelerate weight loss (GLP-1 analogs), improve the course of diabetes or heart failure (SGLT-2 inhibitors), or taper inflammation in steatohepatitis (vitamin E, pioglitazone, GLP-1 analogs). Other approaches to deal with MASLD are currently under development (e.g., multiple incretin analogs, PPAR agonists).
Therefore, I invite authors to contribute papers, both in vitro and in vivo, depicting the search for novel pathophysiological pathways involved in the development of MASLD, potential preventive measures to reduce the burden of MASLD, and tentative therapeutic targets that might prove useful in the treatment of the disease. Comprehensive reviews that analyze the aforementioned subjects and include compelling areas for further research are also welcome.
Topics of interest include, but are not limited to:
• MASLD
• obesity
• cardiovascular risk factors
• incretins
• GLP-1
• SGLT-2
• vitamin E
• pharmacotherapy of MASLD
• pathophysiology of MASLD
• therapeutic lifestyle change
• steatosis
• steatohepatitis
• liver fibrosis
• liver cirrhosis