Yu-Guo Chen

Shandong University, Jinan, Shandong Sheng, China

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Publications (33)85.15 Total impact

  • Article: Usefulness of angiotensin-(1-7) to predict myocardial salvage after percutaneous coronary intervention in patients with acute myocardial infarction.
    International journal of cardiology 03/2013; · 7.08 Impact Factor
  • Article: Poly(ADP-ribose) polymerase inhibition prevents reactive oxygen species induced inhibition of aldehyde dehydrogenase 2 activity.
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    ABSTRACT: Lipid peroxidation plays a critical role in cardiovascular diseases. Aldehydes are the major end products of lipid peroxidation and can be metabolized into less reactive chemical species by aldehyde dehydrogenase 2 (ALDH2). However, ALDH2 dehydrogenase activity can be affected by many factors including reactive oxygen species. To elucidate how reactive oxygen species inhibit ALDH2 dehydrogenase activity, we stimulated human aortic endothelial cells (HAECs) with oxidized low-density lipoproteins (ox-LDL) and performed a myocardial ischemia-reperfusion model. Ox-LDL treatment and ischemia-reperfusion injury inhibited ALDH2 dehydrogenase activity. Poly(ADP-ribose) polymerase (PARP) was activated by ox-LDL stimulation and ischemia-reperfusion injury and PARP inhibition partly restored ALDH2 dehydrogenase activity in ox-LDL treated HAECs and ischemia-reperfusion rat hearts. SIRT3 was upregulated by ox-LDL stimulation and ischemia-reperfusion injury and downregulated by PARP inhibition. Using siRNA to knock downSIRT3, we demonstrated that SIRT3 mediated deacetylation decreased ALDH2 dehydrogenase activity and PARP inhibition partly restored ALDH2 dehydrogenase activity through preventing SIRT3 expression and subsequently preserving ALDH2 acetylation.
    Biochimica et Biophysica Acta 11/2012; · 4.66 Impact Factor
  • Article: Myocardial remodeling in rats with metabolic syndrome: role of Rho-kinase mediated insulin resistance.
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    ABSTRACT: Insulin resistance (IR) plays a critical role in metabolic syndrome (MS). Previous studies have demonstrated that activated ROCK is increased in MS patients. However, the effect of Rho-kinase (ROCK) on IR has not been definitely determined. Thus, the aims of the present study were to determine whether ROCK activation induces IR or affects myocardial structure and function, as well as the possible mechanisms underlying this process. Wistar rats fed high fat, high glucose and high salt diet sewed as model of MS and we used transmission electron microscopy, echocardiogram technology, and terminal deoxynucleotidyl transferase-mediated DNA nick-end labeling staining to identify any myocardial damage. The protein levels of MYPT-1 (characteristic of ROCK activation), IRS-1 and AKT were analyzed by immunohistochemistry and Western blotting. In hearts from MS rats, we found increased protein levels of phospho-MYPT-1 and phospho-IRS-1 (Ser307) and decreased phospho-AKT compared to levels in normal rats. In conclusion, the results suggest that ROCK-mediated IR is involved in the development of myocardial impairments in MS rats and that this effect is mediated probably via the IRS-1/PI3-kinase/AKT pathway.
    Acta biochimica Polonica 06/2012; 59(2):249-54. · 1.49 Impact Factor
  • Article: Simvastatin exerts cardioprotective effects and inhibits the activity of Rho-associated protein kinase in rats with metabolic syndrome.
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    ABSTRACT: 1. Insulin resistance (IR) is crucially involved in the pathophysiology of metabolic syndrome (MS). The aim of the present study was to investigate the effects of simvastatin on IR in rats with MS. 2. A rat model of MS was established and myocardial damage was examined by transmission electron microscopy. Twenty-two MS rats were divided into two groups of 11 rats each: (i) an MS group; and (ii) a simvastatin-treated MS. Ten Wistar rats were used as controls. The phosphorylation of myosin phosphatase target subunit 1 (MYPT-1), insulin receptor substrate 1 (IRS-1) and Akt were analysed by immunohistochemistry and western blotting. 3. Insulin resistance-induced MS was associated with a significant increase in Rho kinase (ROCK) activity and inhibition of the phosphatidylinositol 3-kinase (PI3-K)/Akt pathway. Decreased levels of phosphorylated (p-) MYPT-1 and p-IRS-1 (Ser(307)) and increased levels of p-Akt were found in hearts from the MS + simvastatin compared with the MS group. These results suggest that simvastatin reduces ROCK activity and increases Akt activity. 4. Simvastatin exerts cardioprotective effects and improves IR, which can be attributed, at least in part, to the inhibition of ROCK and activation of PI3-K/Akt.
    Clinical and Experimental Pharmacology and Physiology 06/2012; 39(9):759-64. · 1.85 Impact Factor
  • Article: The correlation between carotid-femoral pulse wave velocity and composition of the aortic media in CAD patients with or without hypertension.
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    ABSTRACT: To investigate the influence of hypertension on large artery elasticity and the microstructure of the ascending aortic media in patients with coronary artery disease (CAD), and the association between arterial compliance and composition of the ascending aorta. 60 patients with CAD who underwent coronary artery bypass graft surgery were divided into two groups: 30 patients in a hypertension group and 30 patients in a non-hypertension group. Carotid-femoral pulse wave velocity (cfPWV) was measured by an automatic device (Complior, Artech, France). The severity of coronary atherosclerosis was assessed after selective coronary angiography using the Gensini score system. A quantitative study was conducted on ascending aorta specimens by histological and computer image analysis. cfPWV of the hypertension group was higher than that of the non-hypertension group. The relative content of collagen in the ascending aortic media of the hypertension group was higher than that of the non-hypertension group, while the relative content of elastin in the ascending aortic media of the hypertension group was lower than that of the non-hypertension group. cfPWV showed a positive correlation with relative contents of collagen in the ascending aorta and a negative correlation with relative contents of elastin in the ascending aorta in the two groups. Hypertension may raise the contents of collagen and decrease the contents of elastin in the ascending aortic media of patients with CAD, which in turn may decrease the patients' large artery compliance. cfPWV may reflect the quantitative changes of collagen and elastin in the ascending aortic media in CAD patients independently of hypertension.
    Schweizerische medizinische Wochenschrift 01/2012; 142:w13546. · 1.68 Impact Factor
  • Article: Alpha-lipoic Acid ameliorates oxidative stress by increasing aldehyde dehydrogenase-2 activity in patients with acute coronary syndrome.
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    ABSTRACT: Aldehyde dehydrogenase-2 (ALDH2) is the main enzyme responsible for acetaldehyde oxidation in ethanol metabolism and also provides protection against oxidative stress. Alpha-lipoic acid (α-LA), a natural dithiol compound with antioxidant properties, has been reported to increase ALDH2 activity in cultured cells. We analyzed the therapeutic efficacy of α-LA in 63 patients with confirmed acute coronary syndrome (ACS). These patients (52 men and 11 women, with age range 49-72 years) were randomized into two groups: untreated group (n = 30) and α-LA group (n = 33). Patients in the α-LA group were given an intravenous injection of 600 mg α-LA every day for 5 days while the patients in the untreated group were given saline. An isoprostane, 8-iso-prostaglandin F2α (8-iso-PGF2α), one product of arachidonic acid metabolism, was measured as a marker for oxidative stress. The serum levels of 8-iso-PGF2α and ALDH2 activity were determined at admission to the hospital (time 0), and at 24 hours and 1 week after treatment. At 24 hours and 1 week after treatment, ALDH2 activity was significantly higher in the α-LA group than in the untreated group (P < 0.05), whereas the levels of 8-iso-PGF2α were significantly lower in the α-LA group than in the untreated group (all P < 0.05). Importantly, the decrease of 8-iso-PGF2α levels correlated with the increased ALDH2 activity at both 24 hours (r = 0.6234, P < 0.001) and 1 week after treatment (r = -0.3941, P = 0.0014). α-LA may ameliorate oxidative stress through up-regulating ALDH2 activity in patients with ACS.
    The Tohoku Journal of Experimental Medicine 01/2012; 229(1):45-51. · 1.24 Impact Factor
  • Article: Effects of ulinastatin, a urinary trypsin inhibitor, on synaptic plasticity and spatial memory in a rat model of cerebral ischemia/reperfusion injury.
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    ABSTRACT: Established therapies for cerebral ischemia-reperfusion injury are currently limited. The urinary trypsin inhibitor ulinastatin (UTI) is considered cytoprotective against ischemia-reperfusion injury in internal organs through its anti-inflammatory activity. We aimed to investigate the neuroprotective effects of UTI on learning and memory of rats after cerebral ischemia-reperfusion injury. Rats were treated with UTI at 10,000 U/kg body weight, then underwent ischemia and reperfusion by the middle cerebral arterial occlusion (MCAO) method. At various times after the onset of reperfusion, we evaluated neurologic impairment scores. Brain sections underwent immunohistochemical staining for synaptophysin and calcium-binding protein S100β. Other rats underwent the Morris water maze test to determine the effects of UTI on learning and memory. Spatial reference learning and memory were improved with UTI treatment by down-regulating S100β-positive cells and preventing the loss of neural cells. Thus, UTI has a neuroprotective role on synaptic plasticity and spatial memory with cerebral ischemia-reperfusion injury in rats.
    The Chinese journal of physiology 12/2011; 54(6):435-42. · 0.56 Impact Factor
  • Article: Efficacy and safety of intensive insulin therapy for critically ill neurologic patients: a meta-analysis.
    Liang Shan, Pan-Pan Hao, Yu-Guo Chen
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    ABSTRACT: Whether intensive insulin therapy (IIT) may improve clinical outcomes for patients admitted to intensive care units, especially critically ill neurologic patients, is still debated. In the present study, we performed a meta-analysis of literature comparing the efficacy and safety of IIT and conventional insulin therapy (CIT) for critically ill neurologic patients in terms of mortality, infection rate, neurologic outcome, and hypoglycemia. We searched for published reports of studies of randomized control trials (up to March 10, 2011) of patients admitted to neurologic intensive care units and investigated an IIT (target of blood glucose control <120 mg/dL) with a control of CIT. Data were abstracted by a standardized protocol. We retrieved reports of five studies involving 924 patients. The risk of mortality, infection rate, and neurologic outcome did not differ with IIT or CIT. However, the incidence of hypoglycemic episodes was significantly higher with IIT than CIT (78.8% vs. 48.9%), with a relative risk of 2.62 (95% confidence interval [CI]: 1.07-6.43; p < 0.04). As compared with CIT, IIT may not benefit critically ill neurologic patients in terms of mortality, infection rate, or neurologic outcome and in fact may be associated with increased hypoglycemic complications. Therefore, IIT cannot be recommended over conventional control for critical neurologic disease, but further study is warranted.
    The Journal of trauma 11/2011; 71(5):1460-4. · 2.48 Impact Factor
  • Article: Role of aldehyde dehydrogenase 2 Glu504lys polymorphism in acute coronary syndrome.
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    ABSTRACT: This study aimed to investigate the association of the aldehyde dehydrogenase 2 (ALDH2) Glu504Lys polymorphism, which exists in 30-50% of East Asians, and risk of acute coronary syndrome (ACS). We enrolled 1092 unrelated Han Chinese, including 546 with ACS and 546 age- and sex-matched controls. Subjects with ALDH2 mutant genotypes showed significantly higher ACS than did controls (46.7% versus 31.9%, P < 0.001). Logistic regression analysis revealed the ALDH2 mutant independently associated with ACS (odds ratio [OR] 1.95, 95% confidence interval [CI]: 1.31-2.92, P = 0.001), but the association was weaker on adjusting for alcohol consumption (OR 1.82, 95% CI: 1.23-2.70, P = 0.003). Similar results were found in a subgroup analysis of patients with primary ST-segment elevation myocardial infarction (STEMI). The ALDH2 mutant was significantly associated with level of high-sensitivity C-reactive protein (hs-CRP) in patients with ACS (P = 0.002) and in controls (P = 0.009) and number of circulating endothelial progenitor cells (EPCs) (P = 0.032); furthermore, inclusion of hs-CRP level and EPCs number as independent variables in regression analysis reduced the importance of ALDH2 polymorphism in ACS or primary STEMI. However, ALDH2 polymorphism was not associated with number of coronary arteries with significant stenosis, Gensini score or flow-mediated dilation of the brachial artery. Our results suggest that ALDH2 mutation is a genetic risk marker for ACS, which is explained in part by alcohol consumption, inflammation and number of circulating EPCs.
    Journal of Cellular and Molecular Medicine 09/2011; 15(9):1955-62. · 4.13 Impact Factor
  • Article: [Roles of monocyte chemoattractant protein-1, RANTES and Fractalkine on promoting vulnerability of atherosclerotic plaques].
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    ABSTRACT: To elucidate the roles of monocyte chemotactic factors (MCP-1, RANTES and Fractalkine) on the vulnerability of atherosclerotic plaques in patients with stable (SAP) and unstable angina pectoris (UAP). Patients with SAP (n = 50) and UAP (n = 50) underwent coronary angiography (CAG) and intravenous ultrasound (IVUS) were included in the study. Monocyte chemotaxis was assayed by the transwell chamber. Concentrations of hs-CRP, MCP-1, RANTES and Fractalkine were measured by Enzyme-linked-immunosorbent assay (ELISA). mRNA expression of MCP-1, RANTES and Fractalkine in the monocytes was detected by RT-PCR. IVUS evidenced soft lipid plaques in 48% UAP patients and in 16% SAP patients (P < 0.05). SAP patients had mainly fibrous and mixed plaques. Plaque burden and vascular remodeling index were significantly higher in UAP patients than in SAP patients (P < 0.01). The averaged number of migrated monocytes in the UAP patients were higher than that in patients with SAP (P < 0.01). Concentration of hs-CRP, MCP-1, RANTES and Fractalkine were significantly higher in UAP patients than those of SAP patients (P < 0.05 or P < 0.01). mRNA expression of MCP-1, RANTES and Fractalkine in patients with UAP was significantly higher than those of SAP patients (P < 0.05). Upregulated monocyte chemotactic factors (MCP-1, RANTES and Fractalkine) might promote coronary plaque vulnerability in UAP patients.
    Zhonghua xin xue guan bing za zhi [Chinese journal of cardiovascular diseases] 09/2011; 39(9):797-801.
  • Article: Association of genetic variants in CYP2C19 and adverse clinical outcomes after treatment with clopidogrel: an updated meta-analysis.
    Thrombosis Research 07/2011; 128(6):593-4. · 2.44 Impact Factor
  • Article: Arginase I attenuates inflammatory cytokine secretion induced by lipopolysaccharide in vascular smooth muscle cells.
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    ABSTRACT: Inflammation plays an important role in atherosclerosis. Arginase I (Arg I) promotes the proliferation of vascular smooth muscle cells; however, the effect of Arg I on inflammation remains unknown. The present study investigated the role of Arg I in inflammation in vitro and in vivo. Quantitative reverse transcription-polymerase chain reaction and Western blot analysis demonstrated that Arg I inhibited tumor necrosis factor-α production induced by lipopolysaccharide in human aortic smooth muscle cells. Inducible nitric oxide synthase substrate competition and nuclear factor-κB activation were main contributors to lipopolysaccharide-mediated inflammatory cytokine generation. However, Arg I could attenuate the function of inducible nitric oxide synthase and inhibit the subsequent nuclear factor-κB activation, leading to inhibition of tumor necrosis factor-α generation. Furthermore, upregulation of Arg I significantly decreased macrophage infiltration and inflammation in atherosclerotic plaque of rabbits, whereas downregulation of Arg I aggravated these adverse effects. The results indicate the antiinflammatory effects of Arg I and suggest an unexpected beneficial role of Arg I in inflammatory disease.
    Arteriosclerosis Thrombosis and Vascular Biology 05/2011; 31(8):1853-60. · 6.37 Impact Factor
  • Article: Meta-analysis of aldehyde dehydrogenase 2 gene polymorphism and Alzheimer's disease in East Asians.
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    ABSTRACT: The association of genetic polymorphism of mitochondrial aldehyde dehydrogenase 2 (ALDH2) and Alzheimer's disease (AD) has been controversial and has been investigated only in several small-sample studies. In the present study, we performed a meta-analysis to evaluate the cross-sectional association of ALDH2 variants and AD risk in East Asian populations. Trials were retrieved through MEDLINE, EMBASE, J-STAGE and the China National Knowledge Internet databases (from January 1, 1994 to November 1, 2010) without any restriction on language. Data were abstracted by a standardized protocol. We found four studies of 821AD patients and 1380 healthy controls that qualified for the analysis. The variant ALDH2 genotype GA/AA was not associated with increased AD risk (odds ratio (OR) = 1.35; 95% confidence interval (CI) = 0.75-2.42; p = 0.32), even after stratification for the status of apolipoprotein E epsilon 4 allele. However, in the subgroup analyses, the association was significant for men (OR = 1.72; 95% CI = 1.10-2.67; p = 0.02). This study adds to the evidence that ALDH2 GA/AA genotype increases the risk of AD among East Asian men, although the effect size is moderate.
    The Canadian journal of neurological sciences. Le journal canadien des sciences neurologiques 05/2011; 38(3):500-6. · 0.97 Impact Factor
  • Article: [Research progress of poly (ADP-ribose) polymerase-1 in cardiac diseases].
    Shu-jian Wei, Bai-lu Wang, Yu-guo Chen
    Zhonghua xin xue guan bing za zhi [Chinese journal of cardiovascular diseases] 01/2011; 39(1):91-3.
  • Article: Images in cardiology. Aberrant origin of circumflex coronary artery from left subclavian artery.
    Journal of the American College of Cardiology 12/2010; 57(1):e1. · 14.16 Impact Factor
  • Article: Endothelial nitric oxide synthase polymorphisms and erectile dysfunction: a meta-analysis.
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    ABSTRACT: Erectile dysfunction (ED) is a common disorder noted for affecting quality of life. Several studies have reported the influence of endothelial nitric oxide synthase (eNOS) polymorphisms on ED susceptibility. However, results of association studies with individually low statistical power are conflicting. Our study aimed to carry out a meta-analysis estimating the association between eNOS variants and the risk of ED. Studies regarding the association between eNOS polymorphisms and ED were searched in Medline and Embase databases. The relevant studies that met the inclusion criteria were eligible for the analysis. Five genetic models and a generalized odds ratio (OR(G) ) were used to estimate the association between eNOS G894T and variable number of 27-bp tandem repeats in intron 4 (4 VNTR) and the risk of ED. Nine articles were included in our meta-analysis. Overall, significant association between the 894T variant and an increased risk of ED was derived for all genetic contrasts except for the recessive model (allele contrast: OR = 1.64, 95% confidence interval [CI]: 1.03-2.60). The meta-analysis based on the OR(G) also produced significant results: OR(G) = 1.64, 95% CI: 1.03-2.61. Significant heterogeneity and publication bias were detected. The cumulative meta-analysis showed the OR increased from 2003 to 2009 and then declined in 2010. Instability in the relative change of OR was observed. Regarding 4 VNTR and its association with ED, the overall analysis showed a lack of significant association (OR = 0.96, 95% CI: 0.72-1.28). No evidence for heterogeneity among studies was observed. Subgroup analysis by ethnicity and recruitment strategy also yielded nonsignificant results. The result supports that G894T variant is associated with an increase in the risk of ED. No evidence for a significant association between 4VNTR and ED is observed. The results of the present meta-analysis should be interpreted with caution. Further confirmation in large and well-designed studies is needed.
    Journal of Sexual Medicine 12/2010; 7(12):3889-98. · 3.55 Impact Factor
  • Article: Association between aldehyde dehydrogenase 2 genetic polymorphism and serum lipids or lipoproteins: a meta-analysis of seven East Asian populations.
    Atherosclerosis 09/2010; 212(1):213-6. · 3.79 Impact Factor
  • Article: Angiotensin II type 1 receptor gene A1166C polymorphism and essential hypertension in Chinese: a meta-analysis.
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    ABSTRACT: We performed a meta-analysis with the aim of assessing the association of the angiotensin II type 1 (AT(1)) receptor gene A1166C polymorphism with essential hypertension in Chinese case-control studies. Studies were searched from the Chinese Biomedicine Database, the China National Knowledge Infrastructure platform, Pubmed and Medline, using the search terms 'hypertension', 'angiotensin II type 1 receptor', 'AT(1)R', 'polymorphism', 'China' and 'Chinese', without limiting to any specific language. The strength of the association between the A1166C polymorphism and hypertension was evaluated by the odds ratio (OR) with the corresponding 95% confidence interval (CI). The analyses were performed with Cochrane RevMan software version 4.2. Overall, the variant genotype AC/CC was associated with a statistically increased essential hypertension risk with the pooled OR 1.48 (95% CI: 1.20-1.83). In the subgroup analyses, the association was also significant among studies using Northern populations, Southern populations, Han Chinese and hospital-based controls. The age did not influence the relationship between the AT( 1) receptor A1166C polymorphism and hypertension in the subgroup analyses. The present meta-analysis suggests that the AT(1) receptor 1166 AC/CC genotype is associated with susceptibility to hypertension in the Chinese population.
    Journal of Renin-Angiotensin-Aldosterone System 03/2010; 11(2):127-35. · 2.44 Impact Factor
  • Article: Efficacy and safety of drug-eluting stents in patients with acute ST-segment-elevation myocardial infarction: a meta-analysis of randomized controlled trials.
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    ABSTRACT: We compared the efficacy and safety of drug-eluting stents with that of bare-metal stents in patients who experienced acute ST-segment-elevation myocardial infarction (STEMI) and underwent primary percutaneous coronary intervention. To do this, we performed a meta-analysis of 13 randomized controlled trials in which drug-eluting stents were compared with bare-metal stents in STEMI patients. The trials involved 6,769 patients (4,246 received drug-eluting stents and 2,523 received bare-metal stents) and follow-up periods of 6 to 48 months. In comparison with bare-metal stents, drug-eluting stents significantly reduced the incidence of major adverse cardiac events, with a risk ratio (RR) of 0.59 (95% confidence interval [CI], 0.47-0.73; P < 0.00001). Drug-eluting stents were not associated with a significant reduction in overall death (RR = 0.94; 95% CI, 0.74-1.20; P = 0.64), but were associated with significant reductions in recurrent myocardial infarction (RR = 0.76; 95% CI, 0.58-0.98; P = 0.03), target-vessel revascularization (RR = 0.47; 95% CI, 0.39-0.56; P <0.00001), and in-stent restenosis (RR = 0.32; 95% CI, 0.25-0.39; P < 0.00001). Moreover, no significant difference was found in the comparative risk of stent thrombosis (RR = 0.85; 95% CI, 0.63-1.14; P = 0.27).On the basis of risk ratio, we conclude that using drug-eluting stents in STEMI patients who undergo primary percutaneous coronary intervention is safe with regard to stent thrombosis within 48 months, and that drug-eluting stents improve clinical outcomes by reducing the risks of major adverse cardiac events, recurrent myocardial infarction, reintervention, and in-stent restenosis, compared with bare-metal stents. However, in order to investigate possible very late stent thrombosis, follow-up of these trials beyond 48 months is warranted.
    Texas Heart Institute journal / from the Texas Heart Institute of St. Luke's Episcopal Hospital, Texas Children's Hospital 01/2010; 37(5):516-24. · 0.65 Impact Factor
  • Article: The polymorphism in aldehyde dehydrogenase-2 gene is associated with elevated plasma levels of high-sensitivity C-reactive protein in the early phase of myocardial infarction.
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    ABSTRACT: Aldehyde dehydrogenase-2 (ALDH2) is a key enzyme of alcohol metabolism, catalyzing the conversion of aldehyde to acetic acid. The G-to-A polymorphism in exon 12 of the ALDH2 gene, which causes Glu-to-Lys substitution at codon 504, has been shown to be an independent risk factor for acute myocardial infarction (AMI). We investigated the possible role of the G-to-A polymorphism in the severity of the myocardial damage in the early phase of AMI by measuring plasma levels of inflammatory markers, including high-sensitivity C-reactive protein (hs-CRP). A total of 226 Han Chinese patients with AMI were divided into two groups: subjects without A allele (GG, n = 144) and subjects with A allele (GA and AA, n = 82), and the blood samples were collected within 12 hours after the onset of AMI. The results displayed that high-density lipoprotein cholesterol (HDL-C) was higher in GG group than that in GA and AA group (p < 0.05). The body mass index (BMI) and the concentration of hs-CRP were lower in GG group than that in GA and AA group (p < 0.05). Multivariate logistic regression analysis showed that subjects with the A allele were at an increased risk for the high level of hs-CRP (> 3 mg/L) compared with those with GG genotype (OR = 4.908, 95% CI = 1.57 approximately 20.98). Thus, the A allele in ALDH2 gene is associated with the elevated plasma levels of hs-CRP after the onset of AMI, suggesting a higher susceptibility of the myocardium to ischemic injuries.
    The Tohoku Journal of Experimental Medicine 01/2010; 221(2):107-12. · 1.24 Impact Factor