ArticleJournal of vascular surgery2005
Genetic analysis of polymorphisms in biologically relevant candidate genes in patients with abdominal aortic aneurysms.
Article in Journal of vascular surgery, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
29 citing papers in PubMed, 117 citations in OpenAlex.
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- Hereditary Aortic Aneurysms and Dissections: Clinical Diagnosis and Genetic Testing.Annals of vascular diseases · 2024Review
- Comparison of Genes Associated with Thoracic and Abdominal Aortic Aneurysms.Aorta (Stamford, Conn.) · 2023Article
- The CCN2 Polymorphism rs12526196 Is a Risk Factor for Ascending Thoracic Aortic Aneurysm.International journal of molecular sciences · 2022Article
- Disturbed nitric oxide signalling gives rise to congenital bicuspid aortic valve and aortopathy.Disease models & mechanisms · 2020Article
- Review
- Relationship of genetic factors with development of aortic dissection and aneurysm.Turk gogus kalp damar cerrahisi dergisi · 2018Article
- Abdominal Aortic Aneurysm: Evolving Controversies and Uncertainties.The International journal of angiology : official publication of the International College of Angiology, Inc · 2018Review
- MicroRNA-181b Controls Atherosclerosis and Aneurysms Through Regulation of TIMP-3 and Elastin.Circulation research · 2017Article
- Genetic and Epigenetic Regulation of Aortic Aneurysms.BioMed research international · 2017Review
- Tissue inhibitor of matrix metalloproteinase-1 polymorphism, plasma TIMP-1 levels, and antihypertensive therapy responsiveness in hypertensive disorders of pregnancy.The pharmacogenomics journal · 2014Article
- Smooth muscle cells from abdominal aortic aneurysms are unique and can independently and synergistically degrade insoluble elastin.Journal of vascular surgery · 2014Article
- TIMP-3 -1296 T>C and TIMP-4 -55 T>C gene polymorphisms play a role in the susceptibility of hepatocellular carcinoma among women.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014Article
- The 372 T/C genetic polymorphism of TIMP-1 is associated with serum levels of TIMP-1 and survival in patients with severe sepsis.Critical care (London, England) · 2013Observational
- Loss of Timp3 gene leads to abdominal aortic aneurysm formation in response to angiotensin II.The Journal of biological chemistry · 2012Article
- Matrix metalloproteinase-9 genotype as a potential genetic marker for abdominal aortic aneurysm.Circulation. Cardiovascular genetics · 2012Article
- Protective effects of angiotensin-converting enzyme I/I and matrix metalloproteinase-3 6A/6A polymorphisms on dilatative pathology within the ascending thoracic aorta.European journal of cardio-thoracic surgery : official journal of the European Association for Cardio-thoracic Surgery · 2011Article
- Genes and abdominal aortic aneurysm.Annals of vascular surgery · 2011Review
- Type-specific dysregulation of matrix metalloproteinases and their tissue inhibitors in end-stage heart failure patients: relationship between MMP-10 and LV remodelling.Journal of cellular and molecular medicine · 2011Article
- Analysis of positional candidate genes in the AAA1 susceptibility locus for abdominal aortic aneurysms on chromosome 19.BMC medical genetics · 2011Article
Corrections and comments
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Authors and funding
12 authors at 6 institutions in 5 countries.
Funding
Abstract
backgroundAbdominal aortic aneurysms (AAAs) are characterized by histologic signs of chronic inflammation, destructive remodeling of extracellular matrix, and depletion of vascular smooth muscle cells. We investigated the process of extracellular matrix remodeling by performing a genetic association study with polymorphisms in the genes for matrix metalloproteinases (MMPs), tissue inhibitors of metalloproteinases (TIMPs), and structural extracellular matrix molecules in AAA. Our hypothesis was that genetic variations in one or more of these genes contribute to greater or lesser activity of these gene products, and thereby contribute to susceptibility for developing AAAs.
methodsDNA samples from 812 unrelated white subject (AAA, n = 387; controls, n = 425) were genotyped for 14 polymorphisms in 13 different candidate genes: MMP1(nt-1607), MMP2(nt-955), MMP3(nt-1612), MMP9(nt-1562), MMP10(nt+180), MMP12(nt-82), MMP13(nt-77), TIMP1(nt+434), TIMP1(rs2070584), TIMP2(rs2009196), TIMP3(nt-1296), TGFB1(nt-509), ELN(nt+422), and COL3A1(nt+581). Odds ratios and P values adjusted for gender and country of origin using logistic regression and stratified by family history of AAA were calculated to test for association between genotype and disease status. Haplotype analysis was carried out for the two TIMP1 polymorphisms in male subjects.
resultsAnalyses with one polymorphism per test without interactions showed an association with the two TIMP1 gene polymorphisms (nt+434, P = .0047; rs2070584, P = .015) in male subjects without a family history of AAA. The association remained significant when analyzing TIMP1 haplotypes (chi 2 P = .014 and empirical P = .009). In addition, we found a significant interaction between the polymorphism and gender for MMP10 ( P = .037) in cases without a family history of AAA, as well as between the polymorphism and country of origin for ELN ( P = .0169) and TIMP3 ( P = .0023) in cases with a family history of AAA.
conclusionsThese findings suggest that genetic variations in TIMP1, TIMP3, MMP10, and ELN genes may contribute to the pathogenesis of AAAs. Further work is needed to confirm the findings in an independent set of samples and to study the functional role of these variants in AAA. It is noteworthy that contrary to a previous study, we did not find an association between the MMP9 (nt-1562) polymorphism and AAA, suggesting genetic heterogeneity of the disease. CLINICAL RELEVANCE: Abdominal aortic aneurysms (AAAs) are an important cardiovascular disease, but the genetic and environmental risk factors, which contribute to individual's risk to develop an aneurysm, are poorly understood. Histologically, AAAs are characterized by signs of chronic inflammation, destructive remodeling of the extracellular matrix, and depletion of vascular smooth muscle cells. We hypothesized that genes involved in these events could harbor changes that make individuals more susceptible to developing aneurysms. This study identified significant genetic associations between DNA sequence changes in tissue inhibitor of metalloproteinase 1 (TIMP1), TIMP3, matrix metalloproteinase 10 (MMP10) and elastin (ELN) genes, and AAA. The results will require confirmation using an independent set of samples. After replication it is possible that these sequence changes in combination with other risk factors could be used in the future to identify individuals who are at increased risk for developing an AAA.
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