Abstract
Genetics and epigenetics play a key role in the development of several diseases, including nonalcoholic fatty liver disease (NAFLD). Family studies demonstrate that first degree relatives of patients with NAFLD are at a much higher risk of the disease than the general population. The development of the Genome Wide Association Study (GWAS) technology has allowed the identification of numerous genetic polymorphisms involved in the evolution of diseases (e.g., PNPLA3, MBOAT7). On the other hand, epigenetic changes interact with inherited risk factors to determine an individual’s susceptibility to NAFLD. Modifications of the histones amino-terminal ends are key factors in the maintenance of chromatin structure and gene expression (cAMP-responsive element binding protein H (CREBH) or SIRT1). Activation of SIRT1 showed potential against the physiological mechanisms related to NAFLD. Abnormal DNA methylation represents a starting point for cancer development in NAFLD patients. Besides, the evaluation of circulating miRNA profiles represents a promising approach to assess and non-invasively monitor liver disease severity. To date, there is no approved pharmacologic therapy for NAFLD and the current treatment remains weight loss with lifestyle modification and exercise. In this review, the status of research into relevant genetic and epigenetic modifiers of NAFLD progression will be discussed.
Highlights
In 1980, a number of patients who had histopathological changes indistinguishable from alcoholic liver disease were described for the first time, but in whom alcohol intake was nil or non-significant [1]
Nonalcoholic fatty liver disease (NAFLD) comprises a progressive spectrum of diseases ranging from hepatic steatosis-accumulation of fat in hepatocytes from an initially benign character to nonalcoholic steatohepatitis, characterized by inflammatory infiltrate and hepatocyte damage together with deposition of collagen and fibrosis progression, simple steatosis may promote fibrosis progression [2]
This study provides solid evidence to affirm that the presence of this variant favors the development of NAFLD
Summary
In 1980, a number of patients who had histopathological changes indistinguishable from alcoholic liver disease were described for the first time, but in whom alcohol intake was nil or non-significant [1]. Nonalcoholic fatty liver disease (NAFLD) comprises a progressive spectrum of diseases ranging from hepatic steatosis-accumulation of fat in hepatocytes from an initially benign character to nonalcoholic steatohepatitis, characterized by inflammatory infiltrate and hepatocyte damage (which includes ballooning and cell death) together with deposition of collagen and fibrosis progression, simple steatosis may promote fibrosis progression [2]. This disease is diagnosed in the absence of significant alcohol consumption, presence of other hereditary diseases, consumption of drugs that can induce steatosis and viral infections (hepatitis B and C virus, human immunodeficiency virus (HIV)) [3]. Diagnosing fibrosis represents a key role, since its presence is a major determinant of the natural course of hepatic and extra-hepatic disease
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