A1166C Angiotensin II Type 1 Receptor Gene Polymorphism May Predict Hemodynamic Response to Losartan in Patients with Cirrhosis and Portal Hypertension

Sookoian, Silvia; Castaño, Gustavo Osvaldo; Garcı́a, Silvia; Viudez, Pedro; González, Claudio; Pirola, Carlos José

doi:10.1111/j.1572-0241.2005.41168.x

Cited by 39 publications

(22 citation statements)

References 27 publications

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“…Indeed, in the three trials from which our major conclusions were drawn, the heterogeneity was statistically insignificant when separated by Child Pugh class using individual patient data. The potential contribution of genetic variation in AT1 receptors on heterogeneity could not be evaluated as this was not tested in any of the included studies [23]. Lastly, as with all meta-analyses, this analysis is also limited by the quality of the studies entered into it.…”

Section: Discussionmentioning

confidence: 94%

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Renin–angiotensin–aldosterone inhibitors in the reduction of portal pressure: A systematic review and meta-analysis

Tandon

Abraldes

Berzigotti

et al. 2010

Journal of Hepatology

123

101

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Section: Discussionmentioning

confidence: 94%

“…The full-text of 40 of these potentially relevant articles was reviewed independently. Twenty-two articles were excluded due to the lack of a control group (8/22) [18][19][20][21][22][23][24][25], the lack of HVPG measurements (12/22) [9,[26][27][28][29][30][31][32][33][34][35][36], or because they were review articles (2/22) [37,38] Fig. 1.…”

Section: Searchmentioning

confidence: 99%

Renin–angiotensin–aldosterone inhibitors in the reduction of portal pressure: A systematic review and meta-analysis

Tandon

Abraldes

Berzigotti

et al. 2010

Journal of Hepatology

123

101

View full text Add to dashboard Cite

“…For instance, Sethupathy and coworkers [31] observed that a target site for the hsa-miR-155, within the 3′ UTR of the human AGTR1 gene that contains the SNP rs5186 (also known as A1166C), leads to allele-specific underexpression of AGTR1, suggesting that the abrogation of miR-155 binding elevates the mRNA-AGTR1 levels. Interestingly, abundant data provide strong evidence of an association of the A1166C variant and cardiovascular disease, including hypertension, and therapeutic response to losartan [32].…”

Section: The Role Of Polymorphisms At Microrna Target Sites In the Pamentioning

confidence: 99%

Metabolic Syndrome: From the Genetics to the Pathophysiology

Sookoian

Pirola

2010

Curr Hypertens Rep

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The metabolic syndrome (MS) constitutes a combination of underlying risk factors for an adverse outcome, cardiovascular disease. Thus, the clinical behavior of the MS can be regarded as a whole. Nevertheless, from a pathogenic point of view, understanding of the underlying mechanisms of each MS intermediate phenotype is far beyond their understanding as an integrative process. Systems biology introduces a new concept for revealing the pathogenesis of human disorders and suggests the presence of common physiologic processes and molecular networks influencing the risk of a disease. This paper shows a model of this concept to explain the genetic determinants of MS-associated phenotypes. Based on the hypothesis that common physiologic processes and molecular networks may influence the risk of MS disease components, we propose two systems-biology approaches: a gene enrichment analysis and the use of a protein-protein interaction network. Our results show that a network driven by many members of the nuclear receptor superfamily of proteins, including retinoid X receptor and farnesoid X receptor (FXR), may be implicated in the pathogenesis of the MS by its interactions at multiple levels of complexity with genes associated with metabolism, cell differentiation, and oxidative stress. In addition, we review two alternative genetic mechanisms that are gaining acceptance in the physiopathology of the MS: the regulation of transcriptional and post-transcriptional gene expression by microRNAs and epigenetic modifications such as DNA methylation.

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“…The SNPs studied are intronic, but they may affect transcriptional activity or possibly be in linkage disequilibrium with functional coding variants. It is also possible the AGTR1 SNPs may affect response to treatment with blockers; there is a relationship between rs5182 and therapeutic response to the angiotensin II receptor antagonist losartan in patients with cirrhosis and portal hypertension ( 285 ).…”

Section: Agtr1mentioning

confidence: 99%

Genetic determinants of hepatic steatosis in man

Hooper

Adams

Burnett

2011

Journal of Lipid Research

119

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in childhood in some individuals, with a prevalence of 10% found in an autopsy study of 2-19 year olds from the United States ( 5 ). The prevalence of NAFLD increases with advancing age, with a peak between 40 and 69 years of age ( 2, 6 ).A cut-off of 5.5% hepatic steatosis has been accepted as the threshold to diagnose fatty liver, based on the 95th centile of hepatic fat content in low-risk subjects [normal body mass index (BMI), normal glucose tolerance, lack of excessive alcohol ingestion, and normal liver function tests] ( 1, 7 ). Subjects with NAFLD may have a range of histopathological changes (

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A1166C Angiotensin II Type 1 Receptor Gene Polymorphism May Predict Hemodynamic Response to Losartan in Patients with Cirrhosis and Portal Hypertension

Abstract: These results suggest that there is a relationship between the AT1R A1166C polymorphisms and the therapeutic response to losartan. The genetic testing may be used as a predictive factor of this response.

Cited by 39 publications

References 27 publications

Renin–angiotensin–aldosterone inhibitors in the reduction of portal pressure: A systematic review and meta-analysis

Renin–angiotensin–aldosterone inhibitors in the reduction of portal pressure: A systematic review and meta-analysis

Metabolic Syndrome: From the Genetics to the Pathophysiology

Genetic determinants of hepatic steatosis in man

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