The role of genetic mutation in alcoholic liver disease

Abstract

Abstract Background Alcoholic liver disease (ALD) is the world’s most common type of liver disease caused due to overconsumption of alcohol. The liver supports the best level of tissue damage by hefty drinking since it is the binding site of ethanol digestion. This disease can progress to alcoholic steatohepatitis from alcoholic fatty liver, which implies steatosis has become the most punctual reaction to hefty drinking and is portrayed by the deposition of fat hepatocytes. In addition, steatosis can advance to steatohepatitis, a more extreme, provocative sort of liver damage described by hepatic inflammation. Constant and unnecessary liquor utilization delivers a wide range of hepatic sores, fibrosis and cirrhosis, and sometimes hepatocellular carcinoma. Most people consuming > 40 g of liquor each day create alcoholic fatty liver (AFL); notwithstanding, just a subset of people will grow further developed infection. Hereditary, epigenetic, and non-hereditary components may clarify the impressive interindividual variety in the ALD phenotype. Main body This systematic review is to classify new candidate genes associated with alcoholic liver disorders, such as RASGRF2, ALDH2, NFE2L2, ADH1B, PNPLA3, DRD2, MTHFR, TM6SF2, IL1B, and CYP2E1, MBOAT7 as well as to revise the functions of each gene in its polymorphic sequence. The information obtained from the previously published articles revealed the crucial relationship between the genes and ALD and discussed each selected gene’s mechanism. Conclusion The aim of this review is to highlight the candidate genes associated with the ALD, and the evidence of this study is to deliberate the part of genetic alterations and modifications that can serve as an excellent biological maker, risk predictors, and therapeutic targets for this disease.