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Title

Angiotensinogen gene G-6A polymorphism influences idiopathic pulmonary fibrosisdisease progression

AuthorsMolina-Molina, Maria; Xaubet, Antoni; Pereda, J.; Serrano-Mollar, Anna CSIC ORCID; Rodríguez-Becerra, E.; Morell, Ferran; Picado, César
KeywordsAngiotensin system
Genetics
Interstitial lung disease
Issue Date28-May-2008
PublisherEuropean Respiratory Society
CitationEuropean Respiratory Journal 32(4): 1004–1008 (2008)
AbstractAngiotensin II is a growth factor that plays a key role in the physiopathology of idiopathic pulmonary fibrosis (IPF). A nucleotide substitution of an adenine instead of a guanine (G-6A) in the proximal promoter region of angiotensinogen (AGT), the precursor of angiotensin II, has been associated with an increased gene transcription rate. In order to investigate whether the G-6A polymorphism of the AGT gene is associated with IPF development, severity and progression, the present study utilised a case–control study design and genotyped G-6A in 219 patients with IPF and 224 control subjects. The distribution of G-6A genotypes and alleles did not significantly differ between cases and controls. The G-6A polymorphism of the AGT gene was not associated with disease severity at diagnosis. The presence of the A allele was strongly associated with increased alveolar arterial oxygen tension difference during follow-up, after controlling for the confounding factors. Higher alveolar arterial oxygen tension changes over time were observed in patients with the AA genotype (0.37¡0.7 mmHg (0.049¡0.093 kPa) per month) compared to GA genotype (0.12¡1 mmHg (0.016¡0.133 kPa) per month) and GG genotype (0.2¡0.6 mmHg (0.027¡0.080 kPa) per month). G-6A polymorphism of the angiotensinogen gene is associated with idiopathic pulmonary fibrosis progression but not with disease predisposition. This polymorphism could have a predictive significance in idiopathic pulmonary fibrosis patients.
Publisher version (URL)http://dx.doi.org/10.1183/09031936.00015808
URIhttp://hdl.handle.net/10261/32497
DOI10.1183/09031936.00015808
ISSN0903-1936
E-ISSN1399-3003
Appears in Collections:(IIBB) Artículos

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