Association of Inflammatory Gene Polymorphisms With Ischemic Stroke in a Chinese Han Population

Nan Zhao; Xin Liu; Yongqin Wang; Xiaoqiu Liu; Jiana Li; Litian Yu; Liyuan Ma; Shuyu Wang; Hongye Zhang; Lisheng Liu; Jingbo Zhao; Xingyu Wang

Disclosures

J Neuroinflammation. 2012;9(162) 

In This Article

Background

Stroke is one of the most common causes of mortality and a leading cause of adult disability worldwide.[1] In China, stroke is the leading cause of death, and ischemic stroke accounts for two-thirds of all strokes.[2] To date, although the etiology and mechanisms of stroke have not been well understood, it is considered as a complex multifactorial disorder with an interaction between the individual's genetic background and various environmental factors. Previous studies have demonstrated that high blood pressure, smoking, poor diet, abdominal obesity, and lack of physical activities as five common risk factors associated with 80% of all strokes.[3] However, these conventional stroke risk factors do not fully account for the overall risk of stroke. Growing evidence suggests inflammatory processes play fundamental roles in both the etiology and pathophysiology of ischemic cerebrovascular disease.[4] Inflammatory molecules, as well as single nucleotide polymorphisms (SNPs) of genes encoding inflammatory mediators, contribute to the development and progression of a large number of pathological conditions, including cardiovascular diseases.[5] SNPs of inflammatory genes strongly influence the plasma levels and biological activity of the corresponding proteins, with potentially important clinical implications.[6,7] In this study, we investigated the association between history of ischemic stroke and polymorphisms of genes encoding prototypical inflammatory molecules, such as interleukin 4 (IL-4), interleukin 6 (IL-6), intercellular adhesion molecule 1 (ICAM-1), E-selectin (E-sel), chemokine (C-C motif) ligand 11 (CCL11), lymphotoxin α (LTA), and so on.

Although hypertension is the most significant risk factor for stroke,[3] evidence from animal and human studies has indicated that some genes predisposing to ischemic stroke are independent of blood pressure.[8] In order to better control the confounding effect of blood pressure in ischemic stroke, the case and control subjects were stratified by their hypertension status.

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