The genes that underlie fatty liver disease: The harvest has begun

Weiskirchen, Ralf; Wasmuth, Hermann E.

doi:10.1002/hep.22800

Cited by 13 publications

(4 citation statements)

References 74 publications

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“…A previous study identified that Asians and Hispanics showed a higher degree of steatosis than Whites and other ethnicities [ 20 ]. The prevalence and histological features of NAFLD also have obvious ethnic difference [ 21 , 22 ]. It was well documented that the association between NAFLD and enhanced inflammation only remained significant in white people but not Chinese, African American and Hispanic people after multivariable adjustment [ 23 ].…”

Section: Discussionmentioning

confidence: 99%

Increased risk of cerebrovascular accident related to non-alcoholic fatty liver disease: a meta-analysis

Ze-min

et al. 2017

Oncotarget

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Recent published studies on the association between non-alcoholic fatty liver disease (NAFLD) and cerebrovascular accident (CVA) risk have yielded conflicting findings. The aim of our study was to identify the potential association by pooling all available publications. A total of nine independent studies were included into our study. The pooled odd ratio (OR) with 95% confidence interval (95% CI) was calculated to weigh the strength for the relationship between NAFLD and CVA risk. We also conducted stratified analyses by study design, ethnicity and disease classification for further elucidation. The pooled results of the present meta-analysis showed that NAFLD was related to increased risk of CVA (OR = 2.32, 95% CI 1.84–2.93, P < 0.001). Besides, NAFLD is associated with increased risk of CVA among both Caucasians (OR = 2.27, 95% CI 1.77–2.90, P < 0.001) and Asians (OR = 2.81, 95% CI 1.43–5.51, P = 0.003). Moreover, the significant association was also observed in case-control studies (OR = 2.73, 95% CI 1.67–4.48, P < 0.001) and cohort studies (OR = 2.22, 95% CI 1.71–2.89, P < 0.001), respectively. In addition, NAFLD was shown to correlate with increased risk of cerebral hemorrhage (OR = 1.85, 95% CI 1.05–3.27, P = 0.034) and the ischemic stroke (OR = 2.51, 95% CI 1.92–3.28, P < 0.001). In conclusion, our findings firstly provide strong evidence for a risk effect of NAFLD on CVA development.

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Section: Discussionmentioning

confidence: 99%

Increased risk of cerebrovascular accident related to non-alcoholic fatty liver disease: a meta-analysis

Ze-min

et al. 2017

Oncotarget

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“…Romeo and colleagues 80 recently reported that homozygotes for a particular PNPLA3 polymorphism were more likely to have steatosis and evidence of cell injury. 81 Moreover, the allele was more common among Hispanic Americans compared with African Americans, indicating that this allele may be a major determinant of ethnic variation. Although its role relative to other genetic variables remains to be established, genetic variation in PNPLA3 may prove to be a significant predictor of severe steatosis under conditions of calorie excess.…”

Section: Familial Associations Genetics and Ethnicity In Nafldmentioning

confidence: 98%

Epidemiology and Natural History of Non-Alcoholic Steatohepatitis

Argo

Caldwell

2009

Clinics in Liver Disease

353

260

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“…Although on the horizon, genomewide association studies of defined liver phenotypes are still limited. 34 Therefore, hypothesisfree genetic research has taken advantage of wellcharacterized animal models and large intercrosses of inbred mice to unravel yet unknown genes with a direct impact on liver injury and fibrosis. 35 By this approach, different risk loci for liver fibrosis have been detected.…”

Section: Genetic Evidence For a Role Of Chemokines In Liver Inflammatmentioning

confidence: 99%

Chemokines in Liver Inflammation and Fibrosis

Wasmuth¹,

Tacke²

2010

Semin Liver Dis

147

111

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Chemokines are a class of small chemotactic molecules with cytokine-like functions, which are well known to orchestrate inflammatory responses within different organs. Overall, more than 50 ligands and 19 receptors belong to the network. In recent years, accumulating functional and genetic evidence suggests that chemokines play a critical role in acute and chronic liver diseases, mediating the infiltration of immune cells (monocytes, T-cells) into the injured liver along a concentration gradient. However, chemokines can also directly affect the biology of liver resident cells, such as hepatic stellate cells and hepatocytes during inflammatory and fibrogenic tissue responses. Although the chemokine system has long been considered highly redundant, studies in knockout animals have convincingly demonstrated that single chemokines and chemokine receptors strongly affect the phenotype of toxic and inflammatory liver disease in vivo. However, depending on the model, these effects can be harmful (proinflammatory, profibrogenic) or beneficial (antifibrotic). This aspect of chemokine biology must be understood before these molecules and their receptors are targeted for therapeutic purposes. Here, we summarize current knowledge on the genetic and functional importance of the chemokine network in injury and highlight their potential for intervening in the inflammation and fibrosis that drives liver disease progression.

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The genes that underlie fatty liver disease: The harvest has begun

Abstract: Fallon PG, Richardson EJ, McKenzie GJ, McKenzie AN. Schistosomeinfection of transgenic mice defines distinct and contrasting pathogenic roles for IL-4 and IL-13: IL-13 is a profibrotic agent.

Cited by 13 publications

References 74 publications

Increased risk of cerebrovascular accident related to non-alcoholic fatty liver disease: a meta-analysis

Increased risk of cerebrovascular accident related to non-alcoholic fatty liver disease: a meta-analysis

Epidemiology and Natural History of Non-Alcoholic Steatohepatitis

Chemokines in Liver Inflammation and Fibrosis

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