Emerging genes associated with the progression of nonalcoholic fatty liver disease

Koutsari, Christina; Lazaridis, Konstantinos N.

doi:10.1002/hep.23869

Cited by 12 publications

(6 citation statements)

References 23 publications

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“…Adiponutrin has been suggested to be involved in the pathogenic mechanisms related to non-alcoholic steatohepatitis and more generally to liver fibrosis development. The I148M mutation has been postulated to increase the free fatty acids' disposition, leading, through oxidative stress and cytokines activation, to inflammation and fibrosis of the liver (26,29,36). Thus, the PNPLA3 rs738409 C 4 G polymorphism may be considered a general predisposing genetic factor to end-stage liver disease, independent of the presence of obesity and insulin sensitivity (37).…”

Section: Discussionmentioning

confidence: 99%

PNPLA3 rs738409C/G polymorphism in cirrhosis: relationship with the aetiology of liver disease and hepatocellular carcinoma occurrence

Falleti

Fabris

Cmet

et al. 2011

Liver International

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Section: Discussionmentioning

confidence: 99%

PNPLA3 rs738409C/G polymorphism in cirrhosis: relationship with the aetiology of liver disease and hepatocellular carcinoma occurrence

Falleti

Fabris

Cmet

et al. 2011

Liver International

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“…This association is independent of body mass index, diabetes, alcohol consumption, and ancestry [36][37][38]. Apolipoprotein C3 gene variants (single-nucleotide polymorphisms C482T and T455C) are associated with NAFLD and insulin resistance [39].…”

Section: Genetic and Early Developmental Factorsmentioning

confidence: 99%

Non‐alcoholic fatty liver disease (NAFLD): why you should care, when you should worry, what you should do

Lebovics¹,

Rubin²

2011

Diabetes Metabolism Res

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SummaryFor the diabetologist, non-alcoholic fatty liver disease (NAFLD) is important at both ends of its spectrum. It is an early warning sign of future risk of metabolic syndrome, type 2 diabetes mellitus, and cardiovascular disease. It may also lead to late life-threatening sequela of diabetes mellitus in the event of progression to liver failure or hepatocellular carcinoma. This review will highlight the recent progress in understanding the natural history of non-alcoholic fatty liver disease and in developing a rational approach to its diagnosis, staging, and management. The pandemic prevalence of non-alcoholic fatty liver disease in Western countries necessitates both a high index of suspicion to identify cases and a non-invasive approach to staging, which is best achieved with clinical/biochemical panels and transient elastography. Lifestyle modification is the cornerstone of management. Recent clinical trials provide support for pharmacologic therapies directed at the metabolic syndrome and at protecting the liver but more data are needed. Bariatric surgery is appropriate for high-risk patients who fail conservative management. Patients with liver failure or hepatocellular carcinoma may be candidates for liver transplantation.

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“…Better understanding of the pathogenesis of liver steatosis and its progression to NASH will have a major impact on the prognosis and therapy of NAFLD patients. This is particularly important for individuals affected by NASH given the greater association of NASH than simple steatosis with cirrhosis and hepatocellular carcinoma (Koutsari and Lazaridis 2010).…”

Section: Introductionmentioning

confidence: 99%

Transcriptional networks implicated in human nonalcoholic fatty liver disease

Liu

2015

Mol Genet Genomics

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The transcriptome of nonalcoholic fatty liver disease (NAFLD) was investigated in several studies. However, the implications of transcriptional networks in progressive NAFLD are not clear and mechanisms inducing transition from nonalcoholic simple fatty liver (NAFL) to nonalcoholic steatohepatitis (NASH) are still elusive. The aims of this study were to (1) construct networks for progressive NAFLD, (2) identify hub genes and functional modules in these networks and (3) infer potential linkages among hub genes, transcription factors and microRNAs (miRNA) for NAFLD progression. A systems biology approach by combining differential expression analysis and weighted gene co-expression network analysis (WGCNA) was utilized to dissect transcriptional profiles in 19 normal, 10 NAFL and 16 NASH patients. Based on this framework, 3 modules related to chromosome organization, proteasomal ubiquitin-dependent protein degradation and immune response were identified in NASH network. Furthermore, 9 modules of co-expressed genes associated with NAFL/NASH transition were found. Further characterization of these modules defined 13 highly connected hub genes in NAFLD progression network. Interestingly, 11 significantly changed miRNAs were predicted to target 10 of the 13 hub genes. Characterization of modules and hub genes that may be regulated by miRNAs could facilitate the identification of candidate genes and pathways responsible for NAFL/NASH transition and lead to a better understanding of NAFLD pathogenesis. The identified modules and hub genes may point to potential targets for therapeutic interventions.

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Emerging genes associated with the progression of nonalcoholic fatty liver disease

Cited by 12 publications

References 23 publications

PNPLA3 rs738409C/G polymorphism in cirrhosis: relationship with the aetiology of liver disease and hepatocellular carcinoma occurrence

PNPLA3 rs738409C/G polymorphism in cirrhosis: relationship with the aetiology of liver disease and hepatocellular carcinoma occurrence

Non‐alcoholic fatty liver disease (NAFLD): why you should care, when you should worry, what you should do

Transcriptional networks implicated in human nonalcoholic fatty liver disease

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