2020
DOI: 10.1002/hep.31229
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Genetic Pathways in Nonalcoholic Fatty Liver Disease: Insights From Systems Biology

Abstract: Nonalcoholic fatty liver disease (NAFLD) represents a burgeoning worldwide epidemic whose etiology reflects multiple interactions between environmental and genetic factors. Here, we review the major pathways and dominant genetic modifiers known to be relevant players in human NAFLD and which may determine key components of the heritability of distinctive disease traits including steatosis and fibrosis. In addition, we have employed general assumptions which are based on known genetic factors in NAFLD to build … Show more

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Cited by 98 publications
(115 citation statements)
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“…Genomics data can potentially be used to assess risk for fibrosis progression and response to therapy and is likely to enter the clinical arena in the future. [76][77][78]83 Proteomics data have shown potential to differentiate NAFL from NASH, whereas lipidomics, metabolomics and the gut microbiome assessments have also been helpful in distinguishing stages of fibrosis in NASH. 65,102,103,108,109 These 'omics' approaches require further validation in larger, more heterogeneous cohorts before they can be considered for use in clinical practice.…”
Section: Resultsmentioning
confidence: 99%
“…Genomics data can potentially be used to assess risk for fibrosis progression and response to therapy and is likely to enter the clinical arena in the future. [76][77][78]83 Proteomics data have shown potential to differentiate NAFL from NASH, whereas lipidomics, metabolomics and the gut microbiome assessments have also been helpful in distinguishing stages of fibrosis in NASH. 65,102,103,108,109 These 'omics' approaches require further validation in larger, more heterogeneous cohorts before they can be considered for use in clinical practice.…”
Section: Resultsmentioning
confidence: 99%
“…Extant studies on the genetic component of NAFLD indicate that, after 12 years following the discovery that an allele in a patatin-like phospholipase domain containing 3 (PNPLA3) variant (rs738409 [G], encoding 148M) was associated with increased hepatic fat 17 and NAFLD disease severity, 18 knowledge of the disease heritability is still incomplete. 3,4,12 The correlation between rs738409 and the risk of developing fatty liver, NASH, and fibrosis is perhaps one of the strongest worldwide-replicated effects for a common variant modifying the individual susceptibility of NAFLD and NASH (explaining ~5.3% of the total variance). 3,4,18,19 Indeed, available evidence indicates that homozygous carriers with the G-risk allele of rs738409 present 3.24-fold greater risk of higher liver necroinflammatory scores and 3.2-fold greater risk of developing fibrosis when compared with homozygous CC carriers.…”
Section: Precision Medicine and Large-scale Ge-nome And Exome Sequencmentioning
confidence: 99%
“…The protein encoded by PNPLA3 is a triacylglycerol lipase that mediates triacylglycerol hydrolysis, mostly in adipocytes. 12 The encoded protein, which appears to be membrane-bound, may be involved in the energy usage/storage balance in adipocytes. 12 Figure 3A shows area under the receiver operating characteristics (AUROC; 0.951) for predicted functional processes linked to PNPLA3, in- 57 Tables show the top 10 predictions (the number provided in the first column).…”
Section: Precision Medicine and Large-scale Ge-nome And Exome Sequencmentioning
confidence: 99%
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