Abstract
Coronary heart disease (CHD) is a complex polygenic disease in which gene-environment interactions play a critical role in disease onset and progression. The Intercellular adhesion molecule 1 (ICAM-1) gene E469K polymorphism is one of the most commonly studied polymorphisms in this gene because of its association with CHD risks, but results were conflicting. The PubMed, Embase, and China National Knowledge Infrastructure databases were searched for case–control studies published up to November 2018. Pooled odds ratios (ORs) and 95% confidence intervals (95% CIs) were calculated to assess the association. Eleven eligible studies, comprising 3435 cases and 3199 controls, were included in the meta-analysis. The pooled result showed that the ICAM-1 gene E469K polymorphism was significantly associated with an increased risk of CHD (OR = 1.20, 95% CI = 1.11–1.29, for the allele K versus allele E; OR = 1.66, 95% CI = 1.43–1.92, for the K allele carriers versus EE). Subgroup analysis supported the results in the Chinese populations and in the Caucasian populations. This meta-analysis suggests that the ICAM-1 gene K469E polymorphism is associated with CHD risk and the K allele is a more significant risk factor for developing CHD amongst Chinese and Caucasians populations.
Highlights
Received: 10 June 2018Revised: 10 December 2018Accepted: 08 January 2019Accepted Manuscript Online: Version of Record published: Coronary artery disease (CAD) continues to be a leading cause of morbidity and mortality amongst adults globally and represents a public health challenge in both industrialized and developing countries [1]
The diagnosis of coronary heart disease (CHD) and matched controls was confirmed by coronary angiography according to the World Health Organization criteria for the confirmation of CHD
Intercellular adhesion molecule 1 (ICAM-1) is a ligand for lymphocyte function-associated antigen 1 and integrinβ-2, making it an important player in various inflammatory/immune conditions, including atherosclerosis
Summary
Received: 10 June 2018Revised: 10 December 2018Accepted: 08 January 2019Accepted Manuscript Online: Version of Record published: Coronary artery disease (CAD) continues to be a leading cause of morbidity and mortality amongst adults globally and represents a public health challenge in both industrialized and developing countries [1]. Genetic susceptibility to coronary heart disease (CHD) may be determined by specific polymorphic variants that encode proteins involved in the atherosclerotic processes. The underlying process is today believed to be predominantly mediated by cell-matrix adhesion molecules expressed on the vascular endothelium and on circulating leukocytes in response to several proinflammatory cytokines [2]. Intercellular adhesion molecule 1 (ICAM-1; human rhinovirus receptor) – a member of the large immunoglobulin superfamily – is widely expressed at a basal level and can be up-regulated by proinflammatory cytokines [2]. It is expressed on a surface of the endothelium cells, smooth muscle cells, macrophages, and activated lymphocytes. ICAM-1 plays an important role in the adhesion of circulating leukocytes to the blood vessel wall and transendothelial migration to the vascular intima [3]
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