Special Issue "Non-Alcoholic Steatohepatitis (NASH)"
A special issue of Journal of Clinical Medicine (ISSN 2077-0383). This special issue belongs to the section "Gastroenterology & Hepatopancreatobiliary Medicine".
Deadline for manuscript submissions: closed (29 February 2020).
Interests: innate immunity; intestinal immunity; liver immunity; nuclear receptors; mucosal immunity; intestinal microbiota
Nonalcoholic fatty liver disease (NAFLD) is a common liver disorder with a high prevalence (20–30%) in Western as well as many Eastern countries, thus representing a rapidly growing health problem worldwide. NAFLD includes a spectrum of disorders ranging from non-alcoholic fatty liver (NAFL), a reversible condition caused by a lipid deposition in the hepatocytes, to non-alcoholic steatohepatitis (NASH), characterized by hepatocytes ballooning and inflammatory cell infiltration. Despite its lower prevalence, ranging from 1.5 to 6.5%, NASH is a progressive liver disease associated with an increased significant risk of developing parenchymal fibrosis, hepatic cirrhosis, and hepatocellular carcinoma. Furthermore, both diseases involve an increased risk for developing cardiovascular complications, including coronary heart disease and stroke. NASH could be considered the hepatic manifestation of metabolic syndrome. The development of NASH is associated with the presence of risk factors, such as weight gain, diabetes, hypertension, menopause, and genetic conditions. Over time, obesity is considered a primary cause of NAFLD and NASH. The accumulation of lipid species, in particular fatty acids, in hepatocytes exerts lipotoxic effects that cause progressive parenchymal cell loss, inflammation, and fibrosis in NASH. However, the pathogenesis of NASH is multifactorial, involving environmental factors, in particular excessive caloric intake associated with a genetic predisposition, but requires second hits, represented by insulin resistance and visceral adipose tissue inflammation, which are thought to be central to the pathogenesis of NASH. To date, there are several available rodent models of NAFLD and NASH, whose relevance to the human NASH is imperfect because they have shown substantial heterogeneity of gene and pathway regulation in comparison to human NASH. However, steatohepatitis induced by long-term administration of a high-fat diet (HFD) and fructose leading to steatosis, inflammation, and fibrosis shows a better correlation to human NAFLD and NASH, confirming the importance of preclinical models. Several agents are currently under development for the treatment of NASH in 2019, but there are no approved drugs to treat this condition. In summary, there is an urgent need to develop novel approaches to treat NASH patients.
Prof. Dr. Stefano Fiorucci
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- Bile acids
- Liver lipids
- Liver fibrosis
- Animal models
- Clinical trials
- Metabolic syndrome
- Drug development
- Nuclear receptors
- Cholesterol biosynthesis
- Vascular complications
- Liver cirrhosis
- Bariatric surgery