HSG/Mfn2 gene polymorphism and essential hypertension: A case-control association study in Chinese

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Abstract

Aim: Hyperplasia suppressor gene/mitofusion-2 (HSG/Mfn2) is a hyperplasia suppressor gene and an essential component of mitochondrial fusion machinery; however, the association between the single nucleotide polymorphism (SNP) of HSG/Mfn2 and hypertension is unclear. Methods: In this study, 542 normotensive subjects (NT group) and 539 hypertensive patients (EH group) were screened for an association study between HSG/Mfn2 and hypertension. Results: The results showed that the genotype distribution and allelic frequency of rs873457, rs2336384, rs1474868, rs4846085 and rs2236055 were significantly different (P<0.05 for all) between EH and NT groups, although those of rs4240897 and rs873458 were not. When comparing the dominant model, significant differences still existed (P<0.05 for all). The allelic frequency of rs4240897 was also slightly different between EH and NT groups (P = 0.047). When subgrouped by sex, the genotype distribution and allelic frequency of all the SNPs (except rs873458) were significantly different in male (P<0.05 for all) but not in female groups. For all the SNPs, only the allelic frequency of rs4240897 was obviously different in female NT and EH groups (P<0.01). Logistic regression showed that body mass index and rs873457 were closely associated with BP after adjusting for age. The frequency of the C-G-A-A-A-C-C haplotype was significantly higher in essential hypertensive patients versus control individuals, both in the entire population, in male or female groups (P<0.01 for all). As for other haplotypes, most were only significantly different in the entire population and male subjects. Conclusion: The genetic variations of HSG/Mfn2 may be associated with hypertension in male Chinese.

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Wang, Z., Liu, Y., Liu, J., Liu, K., Wen, J., Wen, S., & Wu, Z. (2011). HSG/Mfn2 gene polymorphism and essential hypertension: A case-control association study in Chinese. Journal of Atherosclerosis and Thrombosis, 18(1), 24–31. https://doi.org/10.5551/jat.5611

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