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dc.contributor.author
Vilar Gomez, Eduardo  
dc.contributor.author
Pirola, Carlos José  
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Sookoian, Silvia Cristina  
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Wilson, Laura A.  
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Liang, Tiebing  
dc.contributor.author
Chalasani, Naga  
dc.date.available
2023-06-14T09:57:52Z  
dc.date.issued
2022-04  
dc.identifier.citation
Vilar Gomez, Eduardo; Pirola, Carlos José; Sookoian, Silvia Cristina; Wilson, Laura A.; Liang, Tiebing; et al.; PNPLA3 rs738409 and risk of fibrosis in NAFLD: Exploring mediation pathways through intermediate histological features; John Wiley & Sons; Hepatology (Baltimore, Md.); 76; 5; 4-2022; 1482-1494  
dc.identifier.issn
0270-9139  
dc.identifier.uri
http://hdl.handle.net/11336/200516  
dc.description.abstract
Background and Aims: It is unclear whether rs738409 (p.I148M) missense variant in patatin-like phospholipase domain-containing 3 rs738409 promotes fibrosis development by triggering specific fibrogenic pathways or by creating an unfavorable microenvironment by promoting steatosis, inflammation, and ultimately fibrosis. We tested the hypothesis that intermediate histologic traits, including steatosis, lobular and portal inflammation, and ballooning may determine the effect of rs738409 on liver fibrosis among individuals with biopsy-proven NAFLD. Approach and Results: Causal mediation models including multiple mediators in parallel or sequentially were performed to examine the effect of rs738409, by decomposing its total effect on fibrosis severity into direct and indirect effects, mediated by histology traits in 1153 non-Hispanic White patients. Total effect of rs738409 on fibrosis was β = 0.19 (95% CI: 0.09–0.29). The direct effect of rs738409 on fibrosis after removing mediators’ effects was β = 0.09 (95% CI: 0.01–0.17) and the indirect effect of rs738409 on fibrosis through all mediators' effects were β = 0.010 (95% CI: 0.04–0.15). Among all mediators, the greatest estimated effect size was displayed by portal inflammation (β = 0.09, 95% CI: 0.05–0.12). Among different sequential combinations of histology traits, the path including lobular inflammation followed by ballooning degeneration displayed the most significant indirect effect (β = 0.023, 95% CI: 0.011–0.037). Mediation analysis in a separate group of 404 individuals with biopsy-proven NAFLD from other races and ethnicity showed similar results. Conclusions: In NAFLD, nearly half of the total effect of the rs738409 G allele on fibrosis severity could be explained by a direct pathway, suggesting that rs738409 may promote fibrosis development by activating specific fibrogenic pathways. A large proportion of the indirect effect of rs738409 on fibrosis severity is mediated through portal inflammation.  
dc.format
application/pdf  
dc.language.iso
eng  
dc.publisher
John Wiley & Sons  
dc.rights
info:eu-repo/semantics/restrictedAccess  
dc.rights.uri
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/  
dc.subject
NAFLD  
dc.subject
NASH  
dc.subject
PNPLA3  
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FIBROSIS  
dc.subject.classification
Gastroenterología y Hepatología  
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Medicina Clínica  
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CIENCIAS MÉDICAS Y DE LA SALUD  
dc.title
PNPLA3 rs738409 and risk of fibrosis in NAFLD: Exploring mediation pathways through intermediate histological features  
dc.type
info:eu-repo/semantics/article  
dc.type
info:ar-repo/semantics/artículo  
dc.type
info:eu-repo/semantics/publishedVersion  
dc.date.updated
2023-06-12T13:50:54Z  
dc.journal.volume
76  
dc.journal.number
5  
dc.journal.pagination
1482-1494  
dc.journal.pais
Estados Unidos  
dc.description.fil
Fil: Vilar Gomez, Eduardo. Indiana University. School of Medicine; Estados Unidos  
dc.description.fil
Fil: Pirola, Carlos José. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Médicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Médicas; Argentina  
dc.description.fil
Fil: Sookoian, Silvia Cristina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Médicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Médicas; Argentina  
dc.description.fil
Fil: Wilson, Laura A.. Indiana University. School of Medicine; Estados Unidos  
dc.description.fil
Fil: Liang, Tiebing. Indiana University. School of Medicine; Estados Unidos  
dc.description.fil
Fil: Chalasani, Naga. Indiana University. School of Medicine; Estados Unidos  
dc.journal.title
Hepatology (Baltimore, Md.)  
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/url/https://onlinelibrary.wiley.com/doi/10.1002/hep.32491  
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/doi/http://dx.doi.org/10.1002/hep.32491