Considering that calcium/calmodulin-dependent kinase 4 (CAMK4) plays a pivotal role in blood pressure regulation, we investigated the association between a CAMK4 polymorphism (rs10491334) and hypertension in the Han, Kazak, and Uygur ethnic groups. We studied 1224 patients with hypertension and 967 normotensive controls classified into three ethnic groups (Han, Kazak, and Uygur). The rs10491334 polymorphism was genotyped using a TaqMan® 5'-nuclease assay.
Previous case-control studies on the relationship between the CYP4F2 gene rs2108622 polymorphism and hypertension have produced contrasting results. In this study, we aimed to further evaluate the relationship between the CYP4F2 gene rs2108622 polymorphism and hypertension. We selected four case-control studies related to the CYP4F2 gene rs2108622 polymorphism and hypertension by searching PubMed, EMBase, the Chinese Biomedical Literature Database, and the Wanfang database.
The aim of this study was to examine the possible associations between the KLOTHO G-395A gene polymorphism and hypertension in Chinese nonagenarians and centenarians. The G-395A (rs1207568) in the promoter region of the KLOTHO gene was genotyped using a standard TaqMan allelic discrimination assay. We included 710 participants aged 93.5 ± 3.2 years in the analyses. The expression of the A allele of the KLOTHO G-395A polymorphism was significantly downregulated in the hypertension group compared to the control group (0.137 vs 0.200, P
Mutations in mitochondrial DNA have been found to be associated with hypertension. Of these, mitochondrial transfer RNA (mt-tRNA) is a hot spot for these pathogenic mutations. It is generally believed that these mutations may result in the failure of mt-tRNA metabolism, thereby worsening mitochondrial dysfunction and resulting in hypertension. mt-tRNA is known for its high frequency of polymorphisms and mutations, and the number of reports regarding mt-tRNA mutations and hypertension is increasing significantly.
Hypertension affects one-fifth of the world population. Genome-wide association studies (GWAS) have identified several single nucleotide polymorphisms (SNPs) that correlated with hypertension in large samples. However, the genetic mutations leading to hypertension might differ among various populations, as they have different origins and are subjected to different environmental pressures. Therefore, additional studies are urgently needed to verify the GWAS findings across different populations.
Mounting evidence has implicated the SLC12A3 gene in essential hypertension. Here, we examined the potential associations of common variants of the SLC12A3 gene with blood pressure traits in Mongolians in China. Genomic DNA was extracted from 508 unrelated Mongolian patients with essential hypertension and 246 normotensive Mongolian subjects for genotyping. The genotype distributions of all selected polymorphisms were consistent with Hardy-Weinberg equilibrium.
Acute brain ischemia can induce the activation of c-Jun N-terminal kinases (JNKs). Hypertension is a critical etiology for brain ischemia. We identified the effects of hypertension on the activation of JNK as well as its impact on SP600125, a JNK inhibitor, during endoplasmic reticulum stress (ERS) in the hippocampus using a rat model. Transient whole-brain ischemia was induced by 4-vessel occlusion (bilateral vertebral and bilateral common carotid arteries) in normal and spontaneous hypertensive rats. SP600125 (0.05 mg/kg, iv) was administered 30 min before ischemia.