Relation of Polymorphism of the Histidine Decarboxylase Gene to Chronic Heart Failure in Han Chinese

He, Gong-Hao; Cai, Wen-Ke; Meng, Jingru; Ma, Xue; Zhang, Fan; Lu, Jun; Xu, Gelin

doi:10.1016/j.amjcard.2015.02.062

Cited by 10 publications

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“…A total of 333 randomly selected patients with CHF who were admitted to Kunming General Hospital of Chengdu Military Region between 2012 and 2015 and 354 unrelated, sex-, age-, and ethnicity-matched healthy individuals who had no known cardiovascular-related diseases or hereditary disorders and who were not taking any cardiovascular-related medications were included. The primary inclusion and exclusion criteria for CHF patients are in accordance with our previous report [ 6 ] as well as the Framingham criteria [ 12 ]. Briefly, the inclusion criteria were diagnosis of CHF with abnormal left ventricular function by echocardiography.…”

Section: Methodsmentioning

confidence: 99%

“…Genotyping experiments were performed as previously described [ 6 , 15 , 16 ]. Briefly, the blood samples were collected into tubes containing ethylenediaminetetraacetic acid and stored at −80°C until analysis.…”

Section: Methodsmentioning

confidence: 99%

“…Each SNP frequency in control subjects was tested for departure from Hardy-Weinberg Equilibrium (HWE). Student's t -test, analysis of variance (ANOVA), chi-square (Pearson's χ 2 ) test or Fisher's exact test, and multivariate logistic regression analysis adjusted for age, gender, body mass index (BMI), and traditional cardiovascular risk factors (hypertension, dyslipidemia, diabetes, and smoking habit) under different genetic models were used where necessary according to our previous work [ 6 ]. Odds ratios (ORs) with 95% confidential intervals (CIs) were used to assess the associations between genotypes and CHF risk or clinical variables.…”

Section: Methodsmentioning

confidence: 99%

“…Recently, investigations from different laboratories continuously suggested that cardiac histamine and its related receptor subtypes (e.g., H 2 , and H 3 receptors) played considerable roles during the development of CHF [ 2 – 5 ], indicating that histamine and its related molecules are important factors associated with this disease. Based on these findings, our previous investigation further explored the genetic association between CHF and certain polymorphisms in histidine decarboxylase ( HDC ) gene, which encodes the only rate-limiting enzyme in histamine synthesis, and found that the HDC rs17740607 polymorphism decreased the enzyme activity of HDC, lowered the plasma histamine levels, and was significantly associated with CHF risk [ 6 ], which further strengthened the evidence of histamine involvement in CHF.…”

Section: Introductionmentioning

confidence: 97%

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Associations of Polymorphisms inHRH2,HRH3,DAO,andHNMTGenes with Risk of Chronic Heart Failure

Cai

Zhang

et al. 2016

BioMed Research International

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The pathophysiological functions of cardiac histamine level and related histamine receptors during the development of chronic heart failure (CHF) were intensively investigated previously. However, the relevance of polymorphisms in histamine-related genes, such as HRH2, HRH3, DAO, and HNMT, with CHF remains largely neglected. This study herein aims to analyze the clinical associations of polymorphisms in those genes with CHF risk. A total of 333 unrelated Chinese Han CHF patients and 354 ethnicity-matched healthy controls were recruited and 11 single nucleotide polymorphisms (SNPs) were genotyped. We found that the HRH3 rs3787429 polymorphism was associated with CHF risk (p < 0.001). The T allele of rs3787429 exhibited protective effect against CHF under the dominant (ORs = 0.455; 95% CIs = 0.322–0.642) and additive models (ORs = 0.662; 95% CIs = 0.523–0.838), while, for SNPs in HRH2, DAO, and HNMT, no significant associations were observed in the present study. These findings for the first time screen out one SNP (rs3787429) of HRH3 gene that was significantly associated with CHF in Chinese Han population, which may be a novel biomarker for personal prevention and treatment of CHF and provides novel highlights for investigating the contribution of this disease.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 97%

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Associations of Polymorphisms inHRH2,HRH3,DAO,andHNMTGenes with Risk of Chronic Heart Failure

Cai

Zhang

et al. 2016

BioMed Research International

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“…Chronic heart failure (CHF) is the most common form of heart failure. Whilst most cases of CHF are caused by hypertension, coronary heart disease, and diabetes mellitus, genetic association studies revealed that genetic predispositions contribute greatly to risk and prognosis of CHF [2,3,4,5,6,7,8,9,10]. Nevertheless, the genetic background for sporadic CHF has been poorly characterized yet, and identification of novel risk loci of CHF may help to foster early diagnosis and therapeutic intervention for this disease.…”

Section: Introductionmentioning

confidence: 99%

Basigin rs8259 Polymorphism Confers Decreased Risk of Chronic Heart Failure in a Chinese Population

et al. 2017

IJERPH

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Left ventricular remodeling is an essential risk factor contributing to the pathogenesis of chronic heart failure (CHF). Basigin (BSG) promotes cardiovascular inflammation and myocardial remodeling processes by induction of extracellular matrix metalloproteinases and inflammatory cytokines. BSG rs8259 polymorphism was associated with BSG expression and risk of acute coronary syndrome. Therefore, we investigated whether rs8259 polymorphism contributes to risk and prognosis of CHF in Chinese patients. In total 922 adult patients with CHF and 1107 matched healthy controls were enrolled. BSG rs8259 polymorphism was genotyped using PCR-restriction fragment length polymorphism. Whole blood BSG mRNA expression data from Genotype-Tissue Expression project was accessed. Evaluation of follow-up data was performed in only 15.2% (140) of the patients with CHF. BSG rs8259 TT genotype was associated with a decreased risk of CHF (OR = 0.83, 95% CI = 0.72–0.96, p = 0.010), especially in patients with hypertension (OR = 0.80, 95% CI = 0.68–0.95, p = 0.011) and coronary heart disease (OR = 0.81, 95% CI = 0.69–0.96, p = 0.013) after adjustment for multiple cardiovascular risk factors. Rs8259 T allele was associated with decreased BSG mRNA in whole blood from 338 healthy normal donors (p = 1.31 × 10−6). However, rs8259 polymorphism failed to exhibit an association with cardiovascular mortality (p = 0.283). BSG rs8259 polymorphism may contribute to decreased risk of CHF in a Chinese Han population.

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Histamine H2-receptor antagonism improves conduit artery endothelial function and reduces plasma aldosterone level without lowering arterial blood pressure in angiotensin II–hypertensive mice

Assersen,

Jensen,

Enggaard

et al. 2024

Pflugers Arch - Eur J Physiol

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Aldosterone through the mineralocorticoid receptor MR has detrimental effects on cardiovascular disease. It reduces the bioavailability of nitric oxide and impairs endothelium-dependent vasodilatation. In resistance arteries, aldosterone impairs the sensitivity of vascular smooth muscle cells to nitric oxide by promoting the local secretion of histamine which activates H2 receptors. The present experiments tested in vivo and ex vivo the hypothesis that systemic H2-receptor antagonism reduces arterial blood pressure and improves vasodilatation in angiotensin II–induced chronic hypertension. Hypertension was induced by intravenous infusion of angiotensin II (60 ng kg−1 min−1) in conscious, unrestrained mice infused concomitantly with the H2-receptor antagonist ranitidine (27.8 µg kg−1 min−1) or vehicle for 24 days. Heart rate and arterial blood pressure were recorded by indwelling arterial catheter. Resistance (mesenteric) and conductance (aortae) arteries were harvested for perfusion myography and isometric tension recordings by wire myography, respectively. Plasma was analyzed for aldosterone concentration. ANGII infusion resulted in elevated arterial blood pressure and while in vivo treatment with ranitidine reduced plasma aldosterone concentration, it did not reduce blood pressure. Ranitidine improved ex vivo endothelial function (acetylcholine 10−9 to 10−6 mol L−1) in mesenteric resistance arteries. This was abolished by ex vivo treatment with aldosterone (10−9 mol L−1, 1 h). In aortic segments, in vivo ranitidine treatment impaired relaxation. Activation of histamine H2 receptors promotes aldosterone secretion, does not affect arterial blood pressure, and protects endothelial function in conduit arteries but promotes endothelial dysfunction in resistance arteries during angiotensin II–mediated hypertension. Aldosterone contributes little to angiotensin II–induced hypertension in mice.

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Relation of Polymorphism of the Histidine Decarboxylase Gene to Chronic Heart Failure in Han Chinese

Cited by 10 publications

References 30 publications

Associations of Polymorphisms inHRH2,HRH3,DAO,andHNMTGenes with Risk of Chronic Heart Failure

Associations of Polymorphisms inHRH2,HRH3,DAO,andHNMTGenes with Risk of Chronic Heart Failure

Basigin rs8259 Polymorphism Confers Decreased Risk of Chronic Heart Failure in a Chinese Population

Histamine H2-receptor antagonism improves conduit artery endothelial function and reduces plasma aldosterone level without lowering arterial blood pressure in angiotensin II–hypertensive mice

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