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Article

Renin-angiotensin-aldosterone system (RAAS) gene polymorphism as a risk factor of coronary in-stent restenosis.

Yonsei medical journal - 1 Aug 2002

Ryu Sung Kee, Cho Eun Young, Park Hyun Young, Im Eun Kyoung, Jang Yang Soo, Shin Gil Ja, Shim Won Heum, Cho Seung Yun

Abstract excerpt

Intimal proliferation is a main cause of in-stent restenosis. Over-excretion of angiotensin I converting enzyme (ACE) and aldosterone is reported to stimulate intimal hyperplasia and the genetic effect of these molecules may alter the process of in-stent restenosis. We hypothesized that the genetic polymorphisms that alter the expression of genes such as ACE I/D, CYP11B2-344C/T, and AGT M235T can affect in-stent...

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Share to Angiotensinogen
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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Cytochrome P-450 CYP11B2

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Share to Peptidyl-Dipeptidase A

Share to Polymorphism, Genetic

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Source

Identifiers

PMID: 12205735
DOI: 10.3349/ymj.2002.43.4.461

Genes

ACE
AGT

Variants

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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Renin-angiotensin-aldosterone system (RAAS) gene polymorphism as a risk factor of coronary in-stent restenosis.PMID 12205735Read ↗

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