Genetic and environmental contributions to abdominal aortic aneurysm development in a twin population

Wahlgren, Carl‐Magnus; Larsson, Emma; Magnusson, Patrik K. E.; Hultgren, Rebecka; Swedenborg, Jesper

doi:10.1016/j.jvs.2009.08.036

Cited by 141 publications

(112 citation statements)

References 27 publications

(39 reference statements)

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“…PGI synthase is expressed in vascular cells but not in leukocytes, TxA synthase is mainly expressed in macrophages and platelets, while 5-lipoxygenase and its counterpart FLAP are expressed in leukocytes (mainly polymorphonuclear). We observed an excellent statistical association between the secretion of PGE 2 and PGI 2 , a modest association between PGE 2 and TxA 2, and a lack of association between PGE 2 and LTB 4 . The infl uence of PGI 2 or TxA 2 on PGE 2 levels is unlikely; rather a common cause should underlie these correlations.…”

Section: Ep-4-activation-mediated In Vitro Angiogenesismentioning

confidence: 59%

Microvascular COX-2/mPGES-1/EP-4 axis in human abdominal aortic aneurysm

Camacho

Dilmé

Solà-Villà

et al. 2013

Journal of Lipid Research

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Abdominal aortic aneurysm (AAA) is a late-age onset disorder that affects a high percentage of the population in industrialized countries, and rupture of AAA is associated with high mortality rates ( 1 ). The etiology of AAA is complex with a relevant contribution of genetic factors ( 2 ). Although much effort has been made to clarify the mechanism of AAA development, currently the only effective approach to prevent aneurysm rupture is surgical repair by conventional or endovascular techniques.Evidence has been established for a relationship between atherosclerosis and AAA, both disorders being characterized by an underlying chronic infl ammation . However, there are marked differences between atherosclerotic lesions and AAA. Whereas atherosclerotic plaque is characterized by leukocyte infi ltration at the lumen site and hyperproliferation of vascular smooth muscle cells (VSMCs) causing neointimal hyperplasia, AAA is characterized by leukocyte infi ltration into adventitia and depletion of VSMCs in the media. Other relevant features of AAA are the wall tension strength breakdown caused by proteolytic enzymes progressively destructing elastic fi bers ( 3 ) and hypervascularization of aortic tissue. It has been proposed that this vascularization might contribute to the development and rupture of aneurysms ( 4, 5 ). Abstract We investigated the prostaglandin (PG)E

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Section: Ep-4-activation-mediated In Vitro Angiogenesismentioning

confidence: 59%

Microvascular COX-2/mPGES-1/EP-4 axis in human abdominal aortic aneurysm

Camacho

Dilmé

Solà-Villà

et al. 2013

Journal of Lipid Research

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“…Finding different modes of inheritance in separate collections of families is consistent with AAA being a multifactorial disease, where different loci can have distinct modes of inheritance. A recent twin study also strongly supported the involvement of genetic factors in AAA [30].…”

Section: Genetic Risk Factors For Abdominal Aortic Aneurysmsmentioning

confidence: 72%

Novel Genetic Mechanisms for Aortic Aneurysms

Tromp

Kuivaniemi

Hinterseher

et al. 2010

Curr Atheroscler Rep

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Aortic aneurysms occur in the thoracic and abdominal sections of the aorta and are a deadly late-age-at-onset disease with complex pathobiology. Currently, the number of published genome-wide analyses including microarray-based expression profiling, DNA linkage studies, and genetic association studies is still limited and it is difficult to make generalizations about the disease pathogenesis or genetic risk factors contributing to aortic aneurysms, but it appears that thoracic aortic aneurysms differ in many ways from abdominal aortic aneurysms. Characterization of diseases at the molecular level is likely to lead to more accurate diagnoses and the use of "genomic nosology" of disease. The biggest future challenge will be to translate the genomic information to the clinic and improve our understanding of the disease processes, help us to develop better diagnostic tools, and lead to the design of new ways to manage aortic aneurysms in the era of personalized medicine.

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“…However, it remains unclear which genetic factors influence the formation of AAA in individuals who do not have genetic syndromes or a familial AAA. 9,10 Altered levels of MMPs and TIMPs may be due to differences in the genetic sequences coding these enzymes. Genetic variations can influence the transcription of these genes or the function of the coded proteins.…”

mentioning

confidence: 99%