Abstract
Nonalcoholic fatty liver disease (NAFLD), now the leading cause of liver damage worldwide, is epidemiologically associated with obesity, insulin resistance and type 2 diabetes, and is a potentially progressive condition to advanced liver fibrosis and hepatocellular carcinoma. However, there is huge interindividual variability in liver disease susceptibility. Inherited factors also play an important role in determining disease predisposition. During the last years, common variants in PNPLA3, TM6SF2, MBOAT7 and GCKR have been demonstrated to predispose to the full spectrum of NAFLD pathology by facilitating hepatic fat accumulation in the presence of environmental triggers. Other variants regulating inflammation and fibrogenesis then modulate liver disease progression in those at higher risk. Evidence is also accumulating that rare variants are involved in disease predisposition. In the future, evaluation of genetic risk factors may be exploited to stratify the risk of liver-related complications of the disease, and to guide hepatocellular carcinoma surveillance and choose pharmacological therapy.
Keywords: Cirrhosis, fibrosis of the liver, genetics, hepatocellular carcinoma, nonalcoholic fatty liver disease, nonalcoholic steatohepatitis, steatosis.
Current Pharmaceutical Design
Title:Genetics of Nonalcoholic Fatty Liver Disease: A 2018 Update
Volume: 24 Issue: 38
Author(s): Luca V.C. Valenti*Guido A. Baselli
Affiliation:
- Internal Medicine and Metabolic Diseases, Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico, Department of Pathophysiology and Transplantation, Universita degli Studi di Milano, Milan,Italy
Keywords: Cirrhosis, fibrosis of the liver, genetics, hepatocellular carcinoma, nonalcoholic fatty liver disease, nonalcoholic steatohepatitis, steatosis.
Abstract: Nonalcoholic fatty liver disease (NAFLD), now the leading cause of liver damage worldwide, is epidemiologically associated with obesity, insulin resistance and type 2 diabetes, and is a potentially progressive condition to advanced liver fibrosis and hepatocellular carcinoma. However, there is huge interindividual variability in liver disease susceptibility. Inherited factors also play an important role in determining disease predisposition. During the last years, common variants in PNPLA3, TM6SF2, MBOAT7 and GCKR have been demonstrated to predispose to the full spectrum of NAFLD pathology by facilitating hepatic fat accumulation in the presence of environmental triggers. Other variants regulating inflammation and fibrogenesis then modulate liver disease progression in those at higher risk. Evidence is also accumulating that rare variants are involved in disease predisposition. In the future, evaluation of genetic risk factors may be exploited to stratify the risk of liver-related complications of the disease, and to guide hepatocellular carcinoma surveillance and choose pharmacological therapy.
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Cite this article as:
Valenti V.C. Luca *, Baselli A. Guido , Genetics of Nonalcoholic Fatty Liver Disease: A 2018 Update, Current Pharmaceutical Design 2018; 24 (38) . https://dx.doi.org/10.2174/1381612825666190119113836
DOI https://dx.doi.org/10.2174/1381612825666190119113836 |
Print ISSN 1381-6128 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-4286 |
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