Associations between LPL gene polymorphisms and coronary artery disease: evidence based on an updated and cumulative meta-analysis.

Wen-Qi Ma,Xi-Qiong Han,Ying Wang,Nai-Feng Liu,Yi Zhu

doi:10.1042/bsr20171642

Wen-Qi Ma, Xi-Qiong Han + Show 3 more

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https://doi.org/10.1042/bsr20171642

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Journal: Bioscience reports	Publication Date: Mar 16, 2018
Citations: 9	License type: CC BY 4.0

Affiliation: Zhongda Hospital Southeast University

Abstract

Lipoprotein lipase (LPL) is widely linked to lipid and lipoprotein metabolism, but its effects on coronary artery disease (CAD) are not clearly elucidated. The aim of the present study was to clarify the association between LPL gene polymorphisms and CAD susceptibility. The pooled odds ratio (OR) and 95% confidence interval (CI) were calculated to estimate the strength of the relationship between LPL gene polymorphisms and CAD risk. Comprehensive electronic databases, including PubMed, EMBASE, Web of Science, and the Cochrane Library, were systematically searched. A total of 45 records containing 80 eligible studies were analyzed. The results indicated an increased risk between the LPL D9N polymorphism and susceptibility to CAD in the dominant genetic model (AA + GA vs. GG: OR = 1.46, 95% CI = 1.14–1.87), whereas the LPL HindIII polymorphism showed a protective effect against CAD under all tested models (GG + GT vs. TT: OR = 0.85, 95% CI = 0.75–0.97; GG vs. TT + TG: OR = 0.62, 95% CI = 0.47–0.83; G vs. T: OR = 0.81, 95% CI = 0.71–0.92). No significant association was identified for the LPL N291S and PvuII polymorphisms. Stratification analysis by ethnicity suggested a significant correlation between the LPL S447X polymorphism and CAD susceptibility in Caucasians under the dominant and allele genetic models. In summary, our meta-analysis indicated that the LPL D9N polymorphism was associated with an increased risk of CAD, whereas the S447X and HindIII polymorphisms showed protective effects. There was no association observed between the N291S and PvuII polymorphisms and CAD risk.

Highlights

Coronary artery disease (CAD) is a complex multifactorial disease and a leading cause of morbidity and mortality worldwide [1]
Several studies have demonstrated a causal link between triglyceride-rich lipoproteins (TRLs) and CAD, with variants in several crucial genes involved in TRLs metabolism, including lipoprotein lipase (LPL) and its regulators [2,6]
The results indicated a reduced risk of CAD susceptibility associated with the LPL HindIII polymorphism in all tested genetic models (GG + GT vs. TT: odds ratio (OR) = 0.85, 95% confidence interval (CI) = 0.75–0.97; GG vs. TT + TG: OR = 0.62, 95% CI = 0.47–0.83; G vs. T: OR = 0.81, 95% CI = 0.71–0.92) with some evidence of interstudy heterogeneity (Table 1; Figure 2)

Summary

Introduction

Coronary artery disease (CAD) is a complex multifactorial disease and a leading cause of morbidity and mortality worldwide [1]. Atherosclerosis is the underlying cause of CAD, which is primarily characterized by excessive lipid deposition in the endothelium of the vascular tree walls [3]. Several studies have demonstrated a causal link between triglyceride-rich lipoproteins (TRLs) and CAD, with variants in several crucial genes involved in TRLs metabolism, including LPL and its regulators [2,6]. Numerous studies have reported that the LPL gene variants directly affect abnormal lipid and lipoprotein metabolism and c 2018 The Author(s).

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