The effects of epigenetic modification on the occurrence and progression of liver diseases and the involved mechanism

Chen, Liping; Huang, Weifang; Zhang, Zili; Zhang, Feng; Zheng, Shizhong; Kong, Desong

doi:10.1080/17474124.2020.1736042

Cited by 18 publications

(16 citation statements)

References 130 publications

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“…The methylated state of the DNA (39,(91)(92)(93) influences transcriptional activity within the nucleosome. Modifications in the chromatin structure can alter access and binding of transcription factors to the enhancer/promoter sequences of the DNA that are pivotal for transcription (94,95) (Figure 1).…”

Section: Impact Of Dna Methylation On Gene Transcriptionmentioning

confidence: 99%

Epigenetic Aspects and Prospects in Autoimmune Hepatitis

Czaja¹

2022

Front. Immunol.

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The observed risk of autoimmune hepatitis exceeds its genetic risk, and epigenetic factors that alter gene expression without changing nucleotide sequence may help explain the disparity. Key objectives of this review are to describe the epigenetic modifications that affect gene expression, discuss how they can affect autoimmune hepatitis, and indicate prospects for improved management. Multiple hypo-methylated genes have been described in the CD4+ and CD19+ T lymphocytes of patients with autoimmune hepatitis, and the circulating micro-ribonucleic acids, miR-21 and miR-122, have correlated with laboratory and histological features of liver inflammation. Both epigenetic agents have also correlated inversely with the stage of liver fibrosis. The reduced hepatic concentration of miR-122 in cirrhosis suggests that its deficiency may de-repress the pro-fibrotic prolyl-4-hydroxylase subunit alpha-1 gene. Conversely, miR-155 is over-expressed in the liver tissue of patients with autoimmune hepatitis, and it may signify active immune-mediated liver injury. Different epigenetic findings have been described in diverse autoimmune and non-autoimmune liver diseases, and these changes may have disease-specificity. They may also be responses to environmental cues or heritable adaptations that distinguish the diseases. Advances in epigenetic editing and methods for blocking micro-ribonucleic acids have improved opportunities to prove causality and develop site-specific, therapeutic interventions. In conclusion, the role of epigenetics in affecting the risk, clinical phenotype, and outcome of autoimmune hepatitis is under-evaluated. Full definition of the epigenome of autoimmune hepatitis promises to enhance understanding of pathogenic mechanisms and satisfy the unmet clinical need to improve therapy for refractory disease.

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Section: Impact Of Dna Methylation On Gene Transcriptionmentioning

confidence: 99%

Epigenetic Aspects and Prospects in Autoimmune Hepatitis

Czaja¹

2022

Front. Immunol.

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“…Ethanol oxidation by alcohol dehydrogenase and aldehyde dehydrogenase leads to a reduction of the NAD + /NADH ratio, and then disturbs fatty acid oxidation, glycolysis and glucogenesis, and the tricarboxylic acid cycle, contributing to hepatic steatosis; meanwhile, ethanol oxidation by the microsomal ethanol oxidizing system causes excessive reactive oxygen species generation, which further attacks biological macromolecules resulting in liver injury ( Ceni et al, 2014 ). Emerging evidence shows that alcohol-mediated modification on intracellular biological macromolecules, such as RNA, DNA, and protein, as well as epigenetic modification, contributes to the development of ALD ( Smathers et al, 2011 ; Chen et al, 2020 ; Dou et al, 2020 ; Dou et al, 2021 ; Zhang et al, 2021 ).…”

Section: Pathological Mechanism Of Alcoholic Liver Diseasementioning

confidence: 99%

Editorial: Alcohol Consumption and Liver Diseases: From Pathology to Phytotherapy

2022

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Editorial on the Research TopicAlcohol Consumption and Liver Diseases: From Pathology to Phytotherapy Globally, there are 2.4 billion people who consume alcohol with a high proportion of 39.5% of heavy episodic drinkers among them (GBD 2016 Alcohol Collaborators, 2018. Emerging evidence showed that harmful alcohol consumption is associated with more than 200 diseases and injuries, and leads to 3.3 million deaths worldwide annually (Seitz et al., 2018). As an important site for alcohol metabolism, the liver becomes the main target organ of chronic and heavy alcohol consumptioninduced injury, which is referred to as alcoholic liver disease (ALD). The spectrum of ALD develops from steatosis to steatohepatitis, with some individuals ultimately progressing to fibrosis, cirrhosis, and even hepatocellular carcinoma. The perniciousness of ALD has not attracted enough attention, since the incidence rate of ALD in the population is much less than that of other liver diseases, such as non-alcoholic fatty liver disease. But in fact, ALD is the main source of terminal liver disease in clinic. Alcohol is responsible for about 25% of cirrhosis deaths and 30% of all liver cancer deaths annually (Asrani et al., 2021). Considering the significance of ALD on public health, Frontiers in Pharmacology organized this Research Topic entitled "Alcohol Consumption and Liver Diseases: from Pathology to Phytotherapy" to present recent advances in this field.

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“…Epigenetic factors involve mechanisms that affect and regulate gene expression without changes in DNA sequences[ 21 ]. Therefore, gene expression and cell phenotype related to NAFLD might depend on the genetic information encoded by DNA sequences and epigenetic factors[ 22 ]. Figure 1 shows the multifactorial mechanisms implicated in the offspring's NAFLD development.…”

Section: Introductionmentioning

confidence: 99%

Non-alcoholic fatty liver disease and the impact of genetic, epigenetic and environmental factors in the offspring

Wajsbrot¹,

Leite²,

Salles³

et al. 2022

WJG

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Non-alcoholic fatty liver disease (NAFLD) is the most common chronic liver disease worldwide and is strongly associated with metabolic deregulation. More recently, a significant impact of parental NAFLD in the offspring was demonstrated and has been widely discussed. However, pathogenetic pathways implicated in the inheritance by the offspring and relatives are still under debate. Probably, multiple mechanisms are involved as well as in NAFLD pathogenesis itself. Among the multifactorial involved mechanisms, genetic, epigenetic and environmental backgrounds are strongly related to NAFLD development in the offspring. Thus, based on recent evidence from the available literature concerning genetic, epigenetic and environmental disease modifiers, this review aimed to discuss the relationship between parental NAFLD and its impact on the offspring.

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The effects of epigenetic modification on the occurrence and progression of liver diseases and the involved mechanism

Cited by 18 publications

References 130 publications

Epigenetic Aspects and Prospects in Autoimmune Hepatitis

Epigenetic Aspects and Prospects in Autoimmune Hepatitis

Editorial: Alcohol Consumption and Liver Diseases: From Pathology to Phytotherapy

Non-alcoholic fatty liver disease and the impact of genetic, epigenetic and environmental factors in the offspring

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