Prostacyclin Synthase Gene: Implication and Prevention of Cardiovascular Disease

Author: Tomohiro Nakayama

Source: Vascular Disease Prevention, Volume 1, Number 3, November 2004 , pp. 255-261(7)

Publisher: Bentham Science Publishers

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Abstract:

Prostacyclin (PGI2) inhibits platelet aggregation, and vasoconstriction. Prostacyclin synthase (PGIS), a catalyst of PGI2 formation from prostaglandin H2, is widely distributed and predominantly found in vascular endothelial and smooth muscle cells. The PGIS gene is localized to 20q13.11-13 and thought to be a candidate gene for cardiovascular disease. Several mutations and polymorphisms in the gene were reported to be associated with cardiovascular diseases. These results suggest that PGI2 function depends on the different alleles of the PGIS gene and may influence the risk of cardiovascular diseases. Thus, tailor-made management, such as the administration of PGI2 analogs, may be selected on the basis of individual variants of this gene for prevention of cardiovascular diseases.

Keywords: prostacyclin; cardiovascular disease; prevention; polymorphism; mutation; tailor-made managements; beraprost sodium

Document Type: Review article

DOI: http://dx.doi.org/10.2174/1567270043404962

Affiliations: 1: Division of Receptor Biology, Advanced Medical Research Center, Nihon University School of Medicine, Ooyaguchi-kamimachi, 30-1 Itabashi-ku, Tokyo 173-8610, Japan.

Publication date: 2004-11-01

More about this publication?
  • Vascular Disease Prevention publishes reviews as well as original papers to update all those concerned with this topic at the clinical or scientific level. In addition to clinically relevant topics, we consider reviews and original papers dealing with the more scientific aspects of vascular disease prevention. This includes the evaluation of emerging vascular risk factors, research dealing with the pathogenesis of atherosclerosis and the investigation of new treatment options both at the clinical and scientific level (e.g. epidemiology, patient-based studies, experimental models, in vitro experiments or molecular research). Therefore, another function of Vascular Disease Prevention is to bridge the gap between clinical practice and ongoing laboratory-based research.

    In particular, we welcome critical reviews and comments on recent trials. This is a topic that requires regular updates because of the large number of trials published every year.

    Debates are encouraged in the correspondence section of this journal.
    The editorial structure of Vascular Disease Prevention is set up with the aim of dealing with the submitted material as rapidly as possible. Specialist editors will provide a more expert and rapid assessment unlike a more centralized editorial structure.
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