Genetic and Epigenetic Regulation in Nonalcoholic Fatty Liver Disease (NAFLD)

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...

Full description

Bibliographic Details
Authors: Campo, José Antonio del, Gallego Durán, Rocío, Gallego, Paloma, Grande, Lourdes
Format: article
Status:Published version
Publication Date:2018
Country:España
Institution:Universidad de Sevilla (US)
Repository:idUS. Depósito de Investigación de la Universidad de Sevilla
OAI Identifier:oai:idus.us.es:11441/77301
Online Access:https://hdl.handle.net/11441/77301
https://doi.org/10.3390/ijms19030911
Access Level:Open access
Keyword:NAFLD
Genetics
Epigenetics
miRNAs
SIRT1
PNPLA3
id ES_cf549d0ae672b0faad4cb6b2a48bb95e
oai_identifier_str oai:idus.us.es:11441/77301
network_acronym_str ES
network_name_str España
repository_id_str
spelling Genetic and Epigenetic Regulation in Nonalcoholic Fatty Liver Disease (NAFLD)Campo, José Antonio delGallego Durán, RocíoGallego, PalomaGrande, LourdesNAFLDGeneticsEpigeneticsmiRNAsSIRT1PNPLA3Genetics 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 discussedMDPI AGMedicinaCTS532: Unidad de Hepatologia2018info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionapplication/pdfapplication/pdfhttps://hdl.handle.net/11441/77301https://doi.org/10.3390/ijms19030911reponame:idUS. Depósito de Investigación de la Universidad de Sevillainstname:Universidad de Sevilla (US)InglésInternational Journal of Molecular Sciences, 19 (3), 911. info:eu-repo/semantics/openAccessoai:idus.us.es:11441/773012026-06-17T12:51:07Z
dc.title.none.fl_str_mv Genetic and Epigenetic Regulation in Nonalcoholic Fatty Liver Disease (NAFLD)
title Genetic and Epigenetic Regulation in Nonalcoholic Fatty Liver Disease (NAFLD)
spellingShingle Genetic and Epigenetic Regulation in Nonalcoholic Fatty Liver Disease (NAFLD)
Campo, José Antonio del
NAFLD
Genetics
Epigenetics
miRNAs
SIRT1
PNPLA3
title_short Genetic and Epigenetic Regulation in Nonalcoholic Fatty Liver Disease (NAFLD)
title_full Genetic and Epigenetic Regulation in Nonalcoholic Fatty Liver Disease (NAFLD)
title_fullStr Genetic and Epigenetic Regulation in Nonalcoholic Fatty Liver Disease (NAFLD)
title_full_unstemmed Genetic and Epigenetic Regulation in Nonalcoholic Fatty Liver Disease (NAFLD)
title_sort Genetic and Epigenetic Regulation in Nonalcoholic Fatty Liver Disease (NAFLD)
dc.creator.none.fl_str_mv Campo, José Antonio del
Gallego Durán, Rocío
Gallego, Paloma
Grande, Lourdes
author Campo, José Antonio del
author_facet Campo, José Antonio del
Gallego Durán, Rocío
Gallego, Paloma
Grande, Lourdes
author_role author
author2 Gallego Durán, Rocío
Gallego, Paloma
Grande, Lourdes
author2_role author
author
author
dc.contributor.none.fl_str_mv Medicina
CTS532: Unidad de Hepatologia
dc.subject.none.fl_str_mv NAFLD
Genetics
Epigenetics
miRNAs
SIRT1
PNPLA3
topic NAFLD
Genetics
Epigenetics
miRNAs
SIRT1
PNPLA3
description 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
publishDate 2018
dc.date.none.fl_str_mv 2018
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv https://hdl.handle.net/11441/77301
https://doi.org/10.3390/ijms19030911
url https://hdl.handle.net/11441/77301
https://doi.org/10.3390/ijms19030911
dc.language.none.fl_str_mv Inglés
language_invalid_str_mv Inglés
dc.relation.none.fl_str_mv International Journal of Molecular Sciences, 19 (3), 911.
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv application/pdf
application/pdf
dc.publisher.none.fl_str_mv MDPI AG
publisher.none.fl_str_mv MDPI AG
dc.source.none.fl_str_mv reponame:idUS. Depósito de Investigación de la Universidad de Sevilla
instname:Universidad de Sevilla (US)
instname_str Universidad de Sevilla (US)
reponame_str idUS. Depósito de Investigación de la Universidad de Sevilla
collection idUS. Depósito de Investigación de la Universidad de Sevilla
repository.name.fl_str_mv
repository.mail.fl_str_mv
_version_ 1869420072903114752
score 15,300719