Association of gene polymorphisms in FBN1 and TGF-β signaling with the susceptibility and prognostic outcomes of Stanford type B aortic dissection

This study is aimed at investigating the association of Fibrillin-1 (FBN1) and transforming growth factor β (TGF-β) signaling-related gene polymorphisms with the susceptibility of Stanford type B aortic dissection (AD) and its clinical prognostic outcomes. Five single-nucleotide polymorphism (SNPs)...

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Bibliographic Details
Published in:BMC medical genomics 2022-03, Vol.15 (1), p.65-65, Article 65
Main Authors: Sun, Ling, Chang, Yafei, Jiang, Peipei, Ma, Yitong, Yuan, Qinghua, Ma, Xiang
Format: Article
Language:English
Subjects:
Aneurysm, Dissecting - genetics
Aorta
Aortic aneurysms
Aortic dissection
Blood pressure
Cardiovascular disease
Chest
Chest Pain
Cholesterol
Diabetes
Dissection
FBN1
Fibrillin
Fibrillin-1 - genetics
Gene polymorphism
Genes
Genetic Predisposition to Disease
Genotype
Genotype & phenotype
Glucose
GMDR
Growth factors
Hospitals
Humans
Hypertension
Laboratories
Lipoproteins
Marfan syndrome
Medical prognosis
Mutation
Pain
Patients
Polymorphism, Single Nucleotide
Prognosis
Single-nucleotide polymorphism
SNP
Software
TGFB1
TGFB2
Transforming Growth Factor beta - genetics
Transforming growth factor-b
Transforming growth factor-b1
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Summary:This study is aimed at investigating the association of Fibrillin-1 (FBN1) and transforming growth factor β (TGF-β) signaling-related gene polymorphisms with the susceptibility of Stanford type B aortic dissection (AD) and its clinical prognostic outcomes. Five single-nucleotide polymorphism (SNPs) (FBN1rs 145233125, rs201170905, rs11070646, TGFB1rs1800469, and TGFB2rs900) were analyzed in patients with Stanford type B AD (164) and healthy controls (317). Gene-gene and gene-environment interactions were assessed by generalized multifactor dimensionality reduction. A 4-year follow-up was performed for all AD patients. G carriers of FBN1 rs201170905 and TGFB1 rs1800469 have an increased risk of Stanford type B AD. The interaction of FBN1, TGFB1, TGFB2 and environmental promoted to the increased risk of type B AD (cross-validation consistency = 10/10, P = 0.001). Dominant models of FBN1rs145233125 TC + CC genotype (P = 0.028), FBN1 rs201170905 AG + GG (P = 0.047) and TGFB1 rs1800469 AG + GG (P = 0.052) were associated with an increased risk of death of Stanford type B AD. The recessive model of FBN1 rs145233125 CC genotype (P 
ISSN:1755-8794
1755-8794
DOI:10.1186/s12920-022-01213-z