The role of genetic mutation in alcoholic liver disease

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...

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Main Authors: Ranjith Balakrishnan, Vajagathali Mohammed, Ramakrishnan Veerabathiran
Format: Article
Language:English
Published: SpringerOpen 2022-02-01
Series:Egyptian Liver Journal
Subjects:
Online Access:https://doi.org/10.1186/s43066-022-00175-2
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author Ranjith Balakrishnan
Vajagathali Mohammed
Ramakrishnan Veerabathiran
author_facet Ranjith Balakrishnan
Vajagathali Mohammed
Ramakrishnan Veerabathiran
author_sort Ranjith Balakrishnan
collection DOAJ
description 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.
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spelling doaj.art-e7aef404f92543369d917af52b31dc0a2022-12-21T19:33:35ZengSpringerOpenEgyptian Liver Journal2090-62262022-02-0112111810.1186/s43066-022-00175-2The role of genetic mutation in alcoholic liver diseaseRanjith Balakrishnan0Vajagathali Mohammed1Ramakrishnan Veerabathiran2Human Cytogenetics and Genomics Laboratory, Faculty of Allied Health Sciences, Chettinad Hospital and Research Institute, Chettinad Academy of Research and EducationHuman Cytogenetics and Genomics Laboratory, Faculty of Allied Health Sciences, Chettinad Hospital and Research Institute, Chettinad Academy of Research and EducationHuman Cytogenetics and Genomics Laboratory, Faculty of Allied Health Sciences, Chettinad Hospital and Research Institute, Chettinad Academy of Research and EducationAbstract 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.https://doi.org/10.1186/s43066-022-00175-2Alcoholic liver diseaseGene mutationCirrhosisHepatologySteatosis
spellingShingle Ranjith Balakrishnan
Vajagathali Mohammed
Ramakrishnan Veerabathiran
The role of genetic mutation in alcoholic liver disease
Egyptian Liver Journal
Alcoholic liver disease
Gene mutation
Cirrhosis
Hepatology
Steatosis
title The role of genetic mutation in alcoholic liver disease
title_full The role of genetic mutation in alcoholic liver disease
title_fullStr The role of genetic mutation in alcoholic liver disease
title_full_unstemmed The role of genetic mutation in alcoholic liver disease
title_short The role of genetic mutation in alcoholic liver disease
title_sort role of genetic mutation in alcoholic liver disease
topic Alcoholic liver disease
Gene mutation
Cirrhosis
Hepatology
Steatosis
url https://doi.org/10.1186/s43066-022-00175-2
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