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dc.contributor.author
Sookoian, Silvia Cristina
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dc.contributor.author
Pirola, Carlos Jose
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dc.date.available
2015-05-26T20:24:34Z
dc.date.issued
2013-02-07
dc.identifier.citation
Sookoian S; Carlos J Pirola; Systems Biology Elucidates Common Pathogenic Mechanisms between Nonalcoholic and Alcoholic-Fatty Liver Disease; Public Library Science; Plos One; 8; 2013-3; 58895-58899;
dc.identifier.issn
1932-6203
dc.identifier.uri
http://hdl.handle.net/11336/572
dc.description.abstract
The abnormal accumulation of fat in the liver is often related either to metabolic risk factors associated with metabolic syndrome in the absence of alcohol consumption (nonalcoholic fatty liver disease, NAFLD) or to chronic alcohol consumption (alcoholic fatty liver disease, AFLD). Clinical and histological studies suggest that NAFLD and AFLD share pathogenic mechanisms. Nevertheless, current data are still inconclusive as to whether the underlying biological process and disease pathways of NAFLD and AFLD are alike. Our primary aim was to integrate omics and physiological data to answer the question of whether NAFLD and AFLD share molecular processes that lead to disease development. We also explored the extent to which insulin resistance (IR) is a distinctive feature of NAFLD. To answer these questions, we used systems biology approaches, such as gene enrichment analysis, protein?protein interaction networks, and gene prioritization, based on multi-level data extracted by computational data mining. We observed that the leading disease pathways associated with NAFLD did not significantly differ from those of AFLD. However, systems biology revealed the importance of each molecular process behind each of the two diseases, and dissected distinctive molecular NAFLD and AFLD-signatures. Comparative co-analysis of NAFLD and AFLD clarified the participation of NAFLD, but not AFLD, in cardiovascular disease, and showed that insulin signaling is impaired in fatty liver regardless of the noxa, but the putative regulatory mechanisms associated with NAFLD seem to encompass a complex network of genes and proteins, plausible of epigenetic modifications. Gene prioritization showed a cancer-related functional map that suggests that the fatty transformation of the liver tissue is regardless of the cause, an emerging mechanism of ubiquitous oncogenic activation. In conclusion, similar underlying disease mechanisms lead to NAFLD and AFLD, but specific ones depict a particular disease signature that has a different impact on the systemic context.
dc.format
application/pdf
dc.language.iso
eng
dc.publisher
Public Library Science
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dc.rights
info:eu-repo/semantics/openAccess
dc.rights.uri
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.subject
Liver
dc.subject
Fatty Liver
dc.subject
Systems Biology
dc.subject
Alcohol
dc.subject.classification
Ciencias Médicas y de la Salud
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dc.subject.classification
Medicina Clínica
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dc.subject.classification
Gastroenterología y Hepatología
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dc.title
Systems Biology Elucidates Common Pathogenic Mechanisms between Nonalcoholic and Alcoholic-Fatty Liver Disease
dc.type
info:eu-repo/semantics/article
dc.type
info:ar-repo/semantics/artículo
dc.type
info:eu-repo/semantics/publishedVersion
dc.date.updated
2016-03-30 10:35:44.97925-03
dc.journal.volume
8
dc.journal.number
3
dc.journal.pagination
58895-58899
dc.journal.pais
Estados Unidos
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dc.journal.ciudad
San Francisco
dc.description.fil
Fil: Sookoian, Silvia Cristina.
dc.description.fil
Fil: Pirola, Carlos Jose.
dc.journal.title
Plos One
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dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/url/doi:10.1371/journal.pone.0058895
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