Interleukin-6 (IL-6) -174G/C genomic polymorphism contribution to the risk of coronary artery disease in a Chinese population

Abstract

ABSTRACT.To investigate the role of IL-6 polymorphism (-174G/C and -572C/G) in the development of coronary artery disease (CAD), CAD patients (224) and control subjects (260) were recruited between January 2012 and December 2014. Genotyping at IL-6 -174G/C and -572C/G was conducted via polymerase chain reaction coupled to restriction fragment length polymorphism. Results indicated that several disease risk factors were significantly higher in CAD patients as compared to the control subjects. These factors include hypertension (χ 2 = 20.03, P < 0.001), diabetes mellitus (χ 2 = 33.53, P < 0.001), tobacco smoking (χ 2 = 28.17, P < 0.001), body mass indexes (t = 11.39, P < 0.001), total cholesterol (t = 8.25, P < 0.001), low-density lipoprotein cholesterol (t = 7.24, P < 0.001), high-density lipoprotein cholesterol (t = 3.52, P < 0.001), and triglyceride (t = 6.09, P < 0.001). By unconditional logistic regression analysis, we observed that the CC genotype at IL-6 -174G/C was had a 2.32 (95%CI = 1.33-4.06) fold risk of developing CAD compared to the GG genotype. Moreover, IL-6 -174G/C polymorphism was positively associated with the risk of developing CAD in both dominant (OR = 1.63, 95%CI = 1.12-2.38; P = 0.01) and recessive models (OR = 2.18, 95%CI = 1.26-3.77; P = 0.001). However, no statistically significant association was observed between IL-6 -572C/G polymorphism and risk of CAD. In conclusion, IL-6 -174G/C polymorphisms are associated with the pathogenesis of CAD.

The IL-6 rs1800795 and rs1800796 polymorphisms are associated with coronary artery disease risk

“…After removing duplicates and screening title and abstracts, 54 articles were subjected to the full‐text assessment and 12 articles were excluded due to the lack of detailed genotype distribution data. Finally, 37 articles 12‐14,16,24‐56 were included in the qualitative and quantitative synthesis.…”

Interleukin 6 (rs1800795) gene polymorphism is associated with cardiovascular diseases: a meta-analysis of 74 studies with 86,229 subjects

“…After excluding the overlapping articles of the literature search and applying the selection criteria mentioned previously, 74 research articles (Coker et al, 2011[ 14 ]; Banerjee et al, 2008[ 3 ], 2009[ 4 ]; Balding et al, 2004[ 2 ]; Bennet et al, 2003[ 7 ]; Akinyemi et al, 2017[ 1 ]; Humphries et al, 2001[ 31 ], 2007[ 30 ]; Jabir et al, 2017[ 33 ]; Jenny et al, 2002[ 34 ]; Elsaid et al, 2014[ 17 ]; Chiappelli et al, 2005[ 13 ]; Flex et al, 2004[ 20 ]; Karahan et al, 2005[ 37 ]; Li et al, 2015[ 41 ]; Liaquat et al, 2014[ 42 ]; Kelberman et al, 2004[ 38 ]; Kou et al, 2017[ 39 ]; Lalouschek et al, 2006[ 40 ]; Satti et al, 2013[ 63 ]; Sekuri et al 2007[ 64 ]; Sie et al, 2006[ 65 ]; Wang et al, 2015;[ 81 ] Weger et al, 2005[ 82 ]; Yang et al, 2015[ 83 ]; Basso et al, 2002[ 5 ]; Bennermo et al, 2011[ 6 ]; Berg et al, 2009[ 8 ]; Bhanushali et al, 2013[ 9 ]; Buraczynska et al, 2016[ 10 ]; Chakraborty et al, 2013[ 11 ]; Chamorro et al, 2005[ 12 ]; Danielsson et al, 2005[ 15 ]; Densem et al, 2005[ 16 ]; Fan et al, 2011[ 18 ]; Flex et al, 2002[ 21 ]; Galimudi et al, 2014[ 22 ]; George et al, 2004[ 23 ]; Georges et al, 2001[ 24 ]; Ghazouani et al, 2010[ 26 ], 2011[ 25 ]; Greisenegger et al, 2003[ 27 ]; Hongmei et al, 2016[ 28 ]; Jun et al, 2017[ 36 ]; Licastro et al, 2004[ 43 ]; Lieb et al, 2004[ 44 ]; Maitra et al, 2008[ 48 ]; Mao et al, 2016[ 49 ]; Mastana et al, 2017[ 50 ]; Mishra et al, 2013[ 51 ]; Mitrokhin et al, 2017[ 52 ]; Myśliwska et al, 2006[…”

“…In Table 1 (Tab. 1) (References in Table 1: Akinyemi, 2017[ 1 ]; Balding, 2004[ 2 ]; Banerjee, 2008[ 3 ]; Basso, 2002[ 5 ]; Bennermo, 2011[ 6 ]; Bennet, 2003[ 7 ]; Berg, 2009[ 8 ]; Bhanushali, 2013[ 9 ]; Buraczynska, 2016[ 10 ]; Chakraborty, 2013[ 11 ]; Chamorro, 2005[ 12 ]; Chiapelli, 2005[ 13 ]; Coker, 2011[ 14 ]; Danielsson, 2005[ 15 ]; Densem, 2005[ 16 ]; Elsaid, 2014[ 17 ]; Fan, 2011[ 18 ]; Flex, 2002[ 21 ]; Flex, 2004[ 20 ]; Flex, 2007[ 19 ]; Galimudi, 2014[ 22 ]; George, 2004[ 23 ]; Georges, 2001[ 24 ]; Ghazouani, 2010[ 26 ]; Ghazouani, 2011[ 25 ]; Greisenegger, 2003[ 27 ]; Hongmei, 2016[ 28 ]; Humphries, 2001[ 31 ]; Humphries, 2007[ 30 ]; Jabir, 2017[ 33 ]; Jenny, 2002[ 34 ]; Jun, 2017[ 36 ]; Karahan, 2005[ 37 ]; Kelberman, 2004[ 38 ]; Kou, 2017[ 39 ]; Lalouschek, 2006[ 40 ]; Li, 2015[ 41 ]; Liaquat, 2014[ 42 ]; Licastro, 2004[ 43 ]; Lieb, 2004[ 44 ]; Maitra, 2008[ 48 ]; Mao, 2016[ 49 ]; Mastana, 2017[ 50 ]; Mishra[ 51 ], 2013; Mitrokhin, 2017[ 52 ]; Mysliwska, 2006[ 53 ]; Nauck, 2002[ 54 ]; Panoulas, 2009[ 55 ]; Phulukdaree, 2013[ 56 ]; Potacsek, 2007[ 57 ]; Revilla, 2002[ 58 ]; Rios, 2010[ 59 ]; Rosner, 2005[ 60 ]; Salama, 2015[ 61 ]; Sarecka, 2008[ 62 ]; Satti, 2013[ 63 …”

“…Firstly, in the Chinese population, there was no evidence of heterogeneity in the genetic models and rs1800795 was a risk factor due to its association with CVD ( allelic OR=1.36, CI 95%=1.26-1.48, Z p value= <0.0001 (Figure 2 (Fig. 2) ; References in Figure 2: Fan, 2011[ 18 ]; Hongmei, 2016[ 28 ]; Jun, 2017[ 36 ]; Kou, 2017[ 39 ]; Li, 2015[ 41 ]; Mao, 2016[ 49 ]; Sun, 2014[ 72 ]; Tong, 2010[ 75 ]; Tong, 2013[ 76 ]; Wang, 2015[ 81 ]; Yang, 2015[ 83 ]); homozygous OR = 1.91, CI 95%=1.61-2.27, Z p value= <0.0001; heterozygous OR=1.21, CI 95%=1.09-1.34, Z p value= <0.0001; dominant OR= 1.16, CI 95%=1.05-1.27, Z p value= 0.002; recessive OR= 1.78, CI 95%= 1.51-2.10, Z p value <0.0001).…”

“…First, we evaluated the risk of -174 G>C for CAD; under the five models used, a significant association was observed ( allelic : OR=1.14, CI 95%=1.04-1.23, Z p value 0.002; homozygous : OR=1.50, CI 95%=1.28-1.76, Z p value <0.0001; Figure 5 (Fig. 5) ; References in Figure 5: Berg, 2009[ 8 ]; Bhanushali, 2013[ 9 ]; Ghazouani, 2010[ 26 ]; Ghazouani, 2011[ 25 ]; Humphries, 2001[ 31 ]; Jabir, 2017[ 33 ]; Maitra, 2008[ 48 ]; Mao, 2016[ 49 ]; Mastana, 2017[ 50 ]; Mishra, 2013[ 51 ]; Mysliwska, 2006[ 53 ]; Rios, 2010[ 59 ]; Sarecka, 2008[ 62 ]; Sekuri, 2007[ 64 ]; Smith, 2008[ 68 ]; Sun, 2014[ 72 ]; Tong, 2013[ 76 ]; Wang, 2015[ 81 ]; heterozygous : OR=1.10, CI 95%=1.02-1.19, Z p value= 0.013; dominant : OR= 1.23, CI 95%= 1.11-1.35, Z p value <0.0001; recessive OR= 1.31, CI 95%= 1.10-1.56, Z p value =0.002). Then, we evaluated this association in subjects with PAOD and found a protective effect of the -174 G>C polymorphism under the recessive model (OR=0.39, CI 95%=0.26-0.59, Z p value <0.0001; Figure 6 (Fig.…”