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1.
Stem Cell Res Ther ; 11(1): 22, 2020 Jan 09.
Artigo em Inglês | MEDLINE | ID: mdl-31918758

RESUMO

BACKGROUND: Bone marrow mesenchymal stem cell (BMSC) transplantation represents a promising therapeutic strategy for ischemic heart disease. However, its effects are hampered by the poor viability of transplanted cells and the hostile microenvironment of the ischemic region. Insulin-like growth factor-1 (IGF-1) is an important paracrine growth factor of BMSC and plays an important role in the properties of BMSC. Here, we investigated whether overexpressing IGF-1 could enhance the BMSC viability, migration, anti-apoptosis, and protective effects of cardiomyocytes, and explore the underlying mechanisms' focus on the role of the AKT/secreted frizzled-related protein 2 (SFRP2)/ß-catenin pathway. METHODS: We constructed BMSCs overexpressing insulin-like growth factor-1 (BMSCs-IGF-1) or empty vector (BMSCs-NC) using lentivirus, and evaluated cell survival, proliferation, and migration under normoxic and hypoxic conditions. Co-culture of rat cardiomyoblasts with BMSCs was performed to explore the paracrine effect of BMSCs-IGF-1 for rescuing cardiomyoblasts under hypoxia. Transplantation of BMSCs in acute myocardial infarction rats was used to explore the effect of BMSCs-IGF-1 therapy. RESULTS: BMSCs-IGF-1 exhibited a higher cell proliferation rate, migration capacity, and stemness, and were more resistant to apoptosis under hypoxia. Overexpression of IGF-1 upregulated the expression of total and nuclear ß-catenin via the AKT-secreted frizzled-related protein 2 (SFRP2) pathway, which enhanced cell survival. Inhibition of AKT or SFRP2 knockdown by siRNA significantly antagonized the effect of IGF-1 and decreased the expression of ß-catenin. The expression of ß-catenin target genes, including cyclin D1 and c-Myc, were accordingly decreased. Moreover, BMSCs-IGF-1 could rescue cardiomyoblasts from hypoxia-induced apoptosis and preserve cell viability under hypoxia. Transplantation of BMSCs-IGF-1 into myocardial infarction rats greatly reduced infarct volume than BMSCs-NC, with significantly greater expression of SFRP2 and ß-catenin. CONCLUSIONS: These results suggest that in BMSCs overexpressing IGF-1, SFRP2 is an important mediator for the enhancement of stem cell viability via activating, rather than antagonizing, the Wnt/ß-catenin pathway.

3.
Arch Med Sci ; 14(3): 629-634, 2018 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-29765452

RESUMO

Introduction: The effects of statins on lipoprotein-associated phospholipase A2 (Lp-PLA2) are controversial, and the present study aimed to investigate whether atorvastatin could reduce Lp-PLA2 in rats with dyslipidemia. Material and methods: A high-fat and high-cholesterol diet was prescribed to produce a dyslipidemia model. Thereafter, low-dose atorvastatin (5 mg/kg/day), high-dose atorvastatin (20 mg/kg/day) or saline (without-treatment group) was prescribed for 14 days. At 6 weeks after dyslipidemia model establishment and 14 days of atorvastatin treatment, fasting venous blood was drawn for biochemical analysis. Between-group differences and Pearson correlation analysis were conducted. Results: Compared to the normal-control group, fasting plasma total cholesterol (TC) and low-density lipoprotein cholesterol (LDL-C) levels were significantly increased in dyslipidemia groups, while plasma nitric oxide (NO) levels were significantly decreased with attendant elevation of plasma C-reactive protein (CRP) and rho-associated kinase 1 (ROCK1) levels (p < 0.05). At 14 days of atorvastatin treatment, compared to the without-treatment group, plasma levels of TC and LDL-C in the high-dose group were significantly reduced (p < 0.05); and compared to low-dose and without-treatment groups, NO up-regulation (1.8 ±1.1 µmol/l), and CRP (-0.8 ±0.4 ng/ml), ROCK1 (-124 ±65 mmol/l) and Lp-PLA2 (-3.8 ±1.2 ng/ml) reduction were more significant in the high-dose group (p < 0.05). Pearson correlation analysis showed that TC (r = 0.365), LDL-C (r = 0.472), CRP (r = 0.501) and ROCK1 (r = 0.675) were positively correlated with Lp-PLA2, while NO (r = -0.378) and atorvastatin (r = -0.511) were negatively correlated with Lp-PLA2. Conclusions: Atorvastatin treatment is beneficial for reducing the Lp-PLA2 level in rats with dyslipidemia, which may be related to reduced ROCK1 expression in a dose-dependent manner.

4.
J Hypertens ; 35(4): 677-688, 2017 04.
Artigo em Inglês | MEDLINE | ID: mdl-28253216

RESUMO

BACKGROUND: Whether white-coat hypertension (WCH) is an innocent phenomenon is controversial. METHOD: In this study, we evaluated the association of WCH and the risk of cardiovascular diseases (CVDs) and mortality, stratified by baseline antihypertensive treatment status. Databases (PubMed, EMBASE, CINAHL Plus, Scopus, and Google Scholar) were searched for prospective studies with data on CVD and total mortality associated with WCH. The primary outcomes were the risk of CVD and total mortality associated with WCH stratified by antihypertensive treatment status. The relative risks of events compared with normotension were calculated. RESULTS: A total of 23 cohorts (20 445 individuals), 11 cohorts (8656 individuals), and 12 cohorts (21 336 individuals) were included for analysis of cardiovascular risk associated with WCH in patients without baseline antihypertensive treatment (untreated), or under antihypertensive treatment (treated) or mixed population (including both untreated and treated patients), respectively. In untreated cohorts, WCH was associated with a 38 and 20% increased risk of CVD and total mortality compared with normotension, respectively. In the mixed population, WCH was associated with a 19 and 50% increased risk of CVD and total mortality. However, in the treated patients, neither the risk of CVD, nor total mortality was increased in WCH. Meta-regression analyses indicated that neither differences of clinic blood pressure, nor out-of-office blood pressure variables were correlated with risk of CVD in WCH. CONCLUSION: We concluded that WCH is associated with long-term risk of CVD and total mortality in patients without antihypertensive treatment. Close follow-up should be performed in WCH patients.


Assuntos
Doenças Cardiovasculares/epidemiologia , Hipertensão do Jaleco Branco/epidemiologia , Adulto , Idoso , Idoso de 80 Anos ou mais , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Fatores de Risco
5.
BMJ ; 355: i5953, 2016 Nov 23.
Artigo em Inglês | MEDLINE | ID: mdl-27881363

RESUMO

OBJECTIVES:  To evaluate associations between different definitions of prediabetes and the risk of cardiovascular disease and all cause mortality. DESIGN:  Meta-analysis of prospective cohort studies. DATA SOURCES:  Electronic databases (PubMed, Embase, and Google Scholar). SELECTION CRITERIA:  Prospective cohort studies from general populations were included for meta-analysis if they reported adjusted relative risks with 95% confidence intervals for associations between the risk of composite cardiovascular disease, coronary heart disease, stroke, all cause mortality, and prediabetes. REVIEW METHODS:  Two authors independently reviewed and selected eligible studies, based on predetermined selection criteria. Prediabetes was defined as impaired fasting glucose according to the criteria of the American Diabetes Association (IFG-ADA; fasting glucose 5.6-6.9 mmol/L), the WHO expert group (IFG-WHO; fasting glucose 6.1-6.9 mmol/L), impaired glucose tolerance (2 hour plasma glucose concentration 7.8-11.0 mmol/L during an oral glucose tolerance test), or raised haemoglobin A1c (HbA1c) of 39-47 mmol/mol : (5.7-6.4%) according to ADA criteria or 42-47 mmol/mol (6.0-6.4%) according to the National Institute for Health and Care Excellence (NICE) guideline. The relative risks of all cause mortality and cardiovascular events were calculated and reported with 95% confidence intervals. RESULTS:  53 prospective cohort studies with 1 611 339 individuals were included for analysis. The median follow-up duration was 9.5 years. Compared with normoglycaemia, prediabetes (impaired glucose tolerance or impaired fasting glucose according to IFG-ADA or IFG-WHO criteria) was associated with an increased risk of composite cardiovascular disease (relative risk 1.13, 1.26, and 1.30 for IFG-ADA, IFG-WHO, and impaired glucose tolerance, respectively), coronary heart disease (1.10, 1.18, and 1.20, respectively), stroke (1.06, 1.17, and 1.20, respectively), and all cause mortality (1.13, 1.13 and 1.32, respectively). Increases in HBA1c to 39-47 mmol/mol or 42-47 mmol/mol were both associated with an increased risk of composite cardiovascular disease (1.21 and 1.25, respectively) and coronary heart disease (1.15 and 1.28, respectively), but not with an increased risk of stroke and all cause mortality. CONCLUSIONS:  Prediabetes, defined as impaired glucose tolerance, impaired fasting glucose, or raised HbA1c, was associated with an increased risk of cardiovascular disease. The health risk might be increased in people with a fasting glucose concentration as low as 5.6 mmol/L or HbA1c of 39 mmol/mol.


Assuntos
Doenças Cardiovasculares/mortalidade , Estado Pré-Diabético/mortalidade , Causas de Morte , Humanos , Estudos Prospectivos , Risco
6.
Clin Exp Hypertens ; 38(2): 166-72, 2016.
Artigo em Inglês | MEDLINE | ID: mdl-26452457

RESUMO

OBJECTIVE: To investigate the effects and mechanisms of amlodipine therapy on endothelium dysfunction induced by angiotensin-II (Ang-II) stimulation. METHODS: Human umbilical vein endothelial cells (HUVECs) were used and divided into five groups: Blank control, Ang-II (10(-6 )mol/L), levorotatory amlodipine (5 × 10(-6 )mol/L) + Ang-II (10(-6 )mol/L), dextrorotatory amlodipine (5 × 10(-6 )mol/L) + Ang-II (10(-6 )mol/L) and racemic amlodipine (5 × 10(-6 )mol/L) + Ang-II (10(-6 )mol/L) groups. Twenty-four hours later, HUVECs were collected for evaluating endothelial nitric oxide synthase (eNOS), p-eNOS, rho-associated kinase 1 (ROCK1), Bcl-2 and Bax expressions. Nitric oxide (NO) concentration within endothelium was also detected. Flow cytometry was conducted to assess HUVECs apoptosis. RESULTS: With 24 hours of Ang-II stimulation, compared to blank control group, expressions of eNOS and p-eNOS and NO production were significantly reduced in Ang-II group (p < 0.05), while adding amlodipine-protected HUVECs from dysfunction induced by Ang-II. In contrast, ROCK1 expression was promoted in Ang-II group (p < 0.05). However, the expression of ROCK1 in each enantiomer of amlodipine group was significantly decreased (p < 0.05). Compared to levorotatory amlodipine group, the magnitude of ROCK1 diminishment in dextrorotatory amlodipine group was more profound (p < 0.05). The pro-survival protein (Bcl-2) was significantly upregulated, while the pro-apoptotic protein (Bax) was significantly downregulated in three amlodipine groups compared to Ang-II group. Flow cytometry revealed that amlodipine therapy could protect HUVECs from apoptosis, and no significant difference between three amlodipine groups was observed. CONCLUSION: Amlodipine could suppress Ang-II-induced endothelial dysfunction and apoptosis through diminishing ROCK1 expression.


Assuntos
Anlodipino/farmacologia , Apoptose/efeitos dos fármacos , Bloqueadores dos Canais de Cálcio/farmacologia , Células Endoteliais da Veia Umbilical Humana/efeitos dos fármacos , Hipertensão/fisiopatologia , Óxido Nítrico Sintase Tipo III/efeitos dos fármacos , Quinases Associadas a rho/efeitos dos fármacos , Angiotensina II/farmacologia , Endotélio Vascular/efeitos dos fármacos , Endotélio Vascular/metabolismo , Endotélio Vascular/fisiopatologia , Células Endoteliais da Veia Umbilical Humana/metabolismo , Humanos , Hipertensão/metabolismo , Óxido Nítrico/metabolismo , Óxido Nítrico Sintase Tipo III/metabolismo , Fosfoproteínas/efeitos dos fármacos , Fosfoproteínas/metabolismo , Proteínas Proto-Oncogênicas c-bcl-2/efeitos dos fármacos , Proteínas Proto-Oncogênicas c-bcl-2/metabolismo , Vasoconstritores/farmacologia , Proteína X Associada a bcl-2/efeitos dos fármacos , Proteína X Associada a bcl-2/metabolismo , Quinases Associadas a rho/metabolismo
9.
Lipids Health Dis ; 14: 41, 2015 May 02.
Artigo em Inglês | MEDLINE | ID: mdl-25934565

RESUMO

BACKGROUND: Asymmetric Dimethylarginine (ADMA) is an inhibitor of endogenous nitric oxide synthase, which is the key synthase for nitric oxide (NO) production. Whether statins could protect endothelium by reducing ADMA concentration is unclear, and whether this effect is associated with the dose of statins usage is also needed further studied. METHODS: Dyslipidemia rat model was produced by giving high-fat and high-cholesterol diet for 8 weeks. Thereafter, low-dose (5 mg/kg body weight/day) and high-dose (20 mg/kg body weight/day) atorvastatin were orally prescribed for 4 weeks. Parameters of interest including lipid profiles, inflammatory and oxidative markers, NO production and plasma levels of ADMA and ADMA concentration of myocardium were evaluated. Liver enzymes and creatinine kinase (CK) were also detected for safety concern. RESULTS: At baseline, all parameters were comparable between the sham and the dyslipidemia groups. At 8 weeks of dyslipidemia establishment, as compared to the sham group, body weight and lipid profiles were significantly elevated, and plasma levels of C-reactive protein (CRP), malondialdehyde (MDA) and ADMA were concomitantly increased in accompanying with NO reduction in the dyslipidemia groups. With 4 weeks of atorvastatin therapy, as compared to the control group, lipid disorders and NO production were improved, and plasma levels of CRP, MDA and ADMA were significantly decreased in the high-dose atorvastatin group. ADMA concentration of cardiac tissues was also significantly reduced in the high-dose atorvastatin group. Notably, there was a trend to similar effects which did not reach statistical significance in the low-dose atorvastatin group when compared to the control group. Liver enzyme and CK were comparable after 4 weeks of atorvastatin therapy between groups. CONCLUSION: In rats with dyslipidemia, atorvastatin therapy could reduce plasma level of ADMA and ADMA concentration in cardiac tissues, and these effects are associated with the dose of atorvastatin therapy.


Assuntos
Atorvastatina/uso terapêutico , Dislipidemias/tratamento farmacológico , Endotélio Vascular/efeitos dos fármacos , Inibidores de Hidroximetilglutaril-CoA Redutases/uso terapêutico , Animais , Arginina/análogos & derivados , Arginina/análise , Arginina/sangue , Glicemia/análise , Colesterol/sangue , HDL-Colesterol/sangue , Creatina Quinase/sangue , Dislipidemias/fisiopatologia , Masculino , Miocárdio/química , Óxido Nítrico/sangue , Ratos , Ratos Sprague-Dawley , Triglicerídeos/sangue
12.
Ann Med ; 46(8): 684-92, 2014 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-25230915

RESUMO

BACKGROUND: Reports on the association of prediabetes with all-cause mortality and cardiovascular mortality are inconsistent. Objective. To evaluate the risk of all-cause and cardiovascular mortality in association with impaired fasting glucose (IFG) and impaired glucose tolerance (IGT). METHODS: Prospective cohort studies with data on prediabetes and mortality were included. The relative risks (RRs) of all-cause and cardiovascular mortality were calculated and reported with 95% confidence intervals (95% CIs). RESULTS: Twenty-six studies were included. The risks of all-cause and cardiovascular mortality were increased in participants with prediabetes defined as IFG of 110-125 mg/dL (IFG 110) (RR 1.12, 95% CI 1.05-1.20; and RR 1.19, 95% CI 1.05-1.35, respectively), IGT (RR 1.33, 95% CI 1.24-1.42; RR 1.23, 95% CI 1.11-1.36, respectively), or combined IFG 110 and/or IGT (RR 1.21, 95% CI 1.11-1.32; RR 1.21, 95% CI 1.07-1.36, respectively), but not when IFG was defined as 100-125 mg/dL (RR 1.07, 95% CI 0.92-1.26; and RR 1.16, 95% CI 0.94-1.42, respectively). CONCLUSIONS: Prediabetes, defined as IFG 110, IGT, or combined IFG 110 and/or IGT, was associated with increased all-cause and cardiovascular mortality.


Assuntos
Doenças Cardiovasculares/mortalidade , Estado Pré-Diabético/sangue , Estado Pré-Diabético/epidemiologia , Glicemia/metabolismo , Causas de Morte , Jejum , Teste de Tolerância a Glucose , Humanos , Estado Pré-Diabético/mortalidade , Medição de Risco
13.
Neurology ; 82(13): 1153-61, 2014 Apr 01.
Artigo em Inglês | MEDLINE | ID: mdl-24623843

RESUMO

OBJECTIVE: In this meta-analysis, we sought to evaluate the association between prehypertension and the risk of stroke. METHODS: We searched PubMed and EMBASE databases for studies with data on prehypertension and stroke. Two independent reviewers assessed the reports and extracted data. Prospective studies were included if they reported multivariate-adjusted relative risks (RRs) with 95% confidence intervals (CIs) for the associations between stroke and prehypertension or its 2 subranges (low-range prehypertension: 120-129/80-84 mm Hg; high-range prehypertension: 130-139/85-89 mm Hg). We conducted subgroup analyses according to blood pressure ranges, stroke type, endpoint, age, sex, ethnicity, and study characteristics. RESULTS: Pooled data included the results of 762,393 participants from 19 prospective cohort studies. Prehypertension increased the risk of stroke (RR 1.66; 95% CI 1.51-1.81) compared with optimal blood pressure (<120/80 mm Hg). In the secondary outcome analyses, even low-range prehypertension increased the risk of stroke (RR 1.44; 95% CI 1.27-1.63), and the risk was greater for high-range prehypertension (RR 1.95; 95% CI 1.73-2.21). The RR was higher with high-range than with low-range prehypertension (p < 0.001). There were no significant differences in any of the subgroup analyses (all p > 0.05). CONCLUSIONS: After adjusting for multiple cardiovascular risk factors, prehypertension is associated with stroke morbidity. Although the increased risk is largely driven by high-range prehypertension, the risk is also increased in people with low-range prehypertension.


Assuntos
Pressão Sanguínea/fisiologia , Pré-Hipertensão/diagnóstico , Pré-Hipertensão/fisiopatologia , Acidente Vascular Cerebral/diagnóstico , Acidente Vascular Cerebral/fisiopatologia , Determinação da Pressão Arterial/métodos , Humanos , Pré-Hipertensão/epidemiologia , Estudos Prospectivos , Fatores de Risco , Acidente Vascular Cerebral/epidemiologia
14.
Lipids Health Dis ; 13: 41, 2014 Mar 01.
Artigo em Inglês | MEDLINE | ID: mdl-24580749

RESUMO

BACKGROUND: Lipoprotein associated phospholipase A2 (Lp-PLA2) is a novel biomarker for cardiovascular risk prediction. Whether increased Lp-PLA2 level is associated with re-stenosis after stent-placement is unclear. METHODS: Totally 326 participants eligible for stent-placement were enrolled and divided into two groups according to baseline Lp-PLA2 levels (named normal and elevated groups). Baseline characteristics and clinical outcomes were compared between normal and elevated groups. The relationships between Lp-PLA2 and other risk factors with re-stenosis were evaluated. RESULTS: Only the between-group difference of Lp-PLA2 was significant (123.2 ± 33.6 ng/mL vs 336.8 ± 85.4 ng/mL, P < 0.001) while other demographic and clinical characteristics between these two groups were comparable. Approximately 55.1% and 58.5% of participants in normal and elevated groups presented with acute coronary syndrome, and the percentage of tri-vessels stenoses was significantly higher in elevated group (40.8% vs 32.1%, P = 0.016). Nearly 96.0% and 94.0% of participants in normal and elevated Lp-PLA2 groups were placed with drug-eluting stents, and the others were with bare-metal stents. After 1 year's follow-up, the incidence of clinical end-points was comparable (13.3% vs 15.4%, P = 0.172). Nevertheless, the incidence of re-stenosis was marginally higher in elevated Lp-PLA2 group (8.5% versus 4.6%, P = 0.047). With multivariate analysis, after adjustment for other risk factors, Lp-PLA2 remained an independent predictor for re-stenosis with a hazard ratio of 1.140. No synergistic effect between Lp-PLA2 and other risk factors for re-stenosis was found. CONCLUSION: Increased Lp-PLA2 level is associated with an increased risk of re-stenosis. Lp-PLA2 assessment may be useful in predicting subjects who are at increased risk for re-stenosis.


Assuntos
1-Alquil-2-acetilglicerofosfocolina Esterase/sangue , Doença da Artéria Coronariana/enzimologia , Reestenose Coronária/enzimologia , Idoso , Doença da Artéria Coronariana/sangue , Doença da Artéria Coronariana/mortalidade , Doença da Artéria Coronariana/cirurgia , Reestenose Coronária/sangue , Reestenose Coronária/mortalidade , Reestenose Coronária/prevenção & controle , Feminino , Seguimentos , Humanos , Masculino , Pessoa de Meia-Idade , Análise Multivariada , Modelos de Riscos Proporcionais , Fatores de Risco , Stents , Resultado do Tratamento
15.
Am Heart J ; 167(2): 160-168.e1, 2014 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-24439976

RESUMO

BACKGROUND: Studies of prehypertension and mortality are controversial after adjusting for other cardiovascular risk factors. This meta-analysis sought to evaluate the association of prehypertension with all-cause and cardiovascular disease (CVD) mortality. METHODS: The PubMed, EMBASE, Cochrane Library databases, and conference proceedings were searched for studies with data on prehypertension and mortality. The relative risks (RRs) of all-cause, CVD, coronary heart disease (CHD), and stroke mortality were calculated and presented with 95% CIs. Subgroup analyses were conducted according to blood pressure, age, gender, ethnicity, follow-up duration, participant number, and study characteristics. RESULTS: Data from 1,129,098 participants were derived from 20 prospective cohort studies. Prehypertension significantly increased the risk of CVD, CHD, and stroke mortality (RR 1.28, 95% CI 1.16-1.40; RR 1.12, 95% CI 1.02-1.23; and RR 1.41, 95% CI 1.28-1.56, respectively), but did not increase the risk of all-cause mortality after multivariate adjustment (RR 1.03, 95% CI 0.97-1.10). The difference between CHD mortality and stroke mortality was significant (P < .001). Subgroup analyses showed that CVD mortality was significantly increased in high-range prehypertension (RR 1.28, 95% CI 1.16-1.41) but not in low-range prehypertension (RR 1.08, 95% CI 0.98-1.18). CONCLUSION: Prehypertension is associated with CVD mortality, especially with stroke mortality, but not with all-cause mortality. The risk for CVD mortality is largely driven by high-range prehypertension.


Assuntos
Pressão Sanguínea/fisiologia , Pré-Hipertensão/mortalidade , Doenças Cardiovasculares/mortalidade , Causas de Morte/tendências , Humanos , Fatores de Risco , Taxa de Sobrevida/tendências
16.
Am J Kidney Dis ; 63(1): 76-83, 2014 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-24074825

RESUMO

BACKGROUND: Studies of the association of prehypertension with the incidence of end-stage renal disease (ESRD) after adjusting for other cardiovascular risk factors have shown controversial results. STUDY DESIGN: Systematic review and meta-analysis of prospective cohort studies. SETTING & POPULATION: Adults with prehypertension. SELECTION CRITERIA FOR STUDIES: Studies evaluating the association of prehypertension with the incidence of ESRD identified by searches in PubMed, EMBASE, and Cochrane Library databases and conference proceedings, without language restriction. PREDICTOR: Prehypertension. OUTCOMES: The relative risks (RRs) of ESRD were calculated and reported with 95% CIs. Subgroup analyses were conducted according to blood pressure (BP), age, sex, ethnicity, and study characteristics. RESULTS: Data from 1,003,793 participants were derived from 6 prospective cohort studies. Compared with optimal BP, prehypertension significantly increased the risk of ESRD (RR, 1.59; 95% CI, 1.39-1.91). In subgroup analyses, prehypertension significantly predicted higher ESRD risk across age, sex, ethnicity, and study characteristics. Even low-range (BP, 120-129/80-84 mm Hg) prehypertension increased the risk of ESRD compared with optimal BP (RR, 1.44; 95% CI, 1.19-1.74), and the risk increased further with high-range (BP, 130-139/85-89 mm Hg) prehypertension (RR, 2.02; 95% CI, 1.70-2.40). The RR was significantly higher in the high-range compared with the low-range prehypertensive population (P = 0.01). LIMITATIONS: No access to individual patient-level data. CONCLUSIONS: Prehypertension is associated with incident ESRD. The increased risk is driven largely by high-range prehypertension.


Assuntos
Falência Renal Crônica , Pré-Hipertensão , Adulto , Idoso , Pressão Sanguínea , Determinação da Pressão Arterial/estatística & dados numéricos , Estudos de Coortes , Feminino , Humanos , Incidência , Falência Renal Crônica/epidemiologia , Falência Renal Crônica/etiologia , Falência Renal Crônica/fisiopatologia , Masculino , Pessoa de Meia-Idade , Pré-Hipertensão/complicações , Pré-Hipertensão/diagnóstico , Pré-Hipertensão/epidemiologia , Pré-Hipertensão/fisiopatologia , Risco , Medição de Risco
17.
PLoS One ; 8(12): e79100, 2013.
Artigo em Inglês | MEDLINE | ID: mdl-24312447

RESUMO

BACKGROUND: Adipose-derived mesenchymal stem cells (ASCs) transplantation is a promising approach for myocardium repair. Promotion of ASCs migration and survival is the key for improving ASCs efficiency. SDF-1α is a critical factor responsible for ASCs migration and survival. Atorvastatin (Ator) is capable of up-regulating SDF-1α. Therefore, we're going to investigate whether ASCs migration and survival could be improved with atorvastatin. METHODS: In vitro study, cardiomyocytes were subjected to anoxia-reoxygenation injury and subsequently divided into different groups: group blank control, Ator, Ator plus L-NAME (A+L-NAME) and Ator plus AMD3100 (A+AMD3100).When migration analysis completed, cardiomyocytes were used for subsequent analyses. In vivo study, rats underwent ischemia-reperfusion injury were assigned into different groups corresponding to in vitro protocols. ASCs were transplanted on the seventh day of atorvastatin therapy. Seven days later, the rates of migration, differentiation and apoptosis were evaluated. RESULTS: Compared with other groups, ASCs migration in vitro was significantly improved in group Ator, which was dependent on SDF-1α/CXCR-4 coupling. Results of in vivo study were consistent with that of in vitro study, further supporting the notion that the efficacy of atorvastatin on ASCs migration improvement was related to SDF-1α/CXCR-4 axis. Higher vessel density in group Ator might be another mechanism responsible for migration improvement. Concomitantly, apoptosis was significantly reduced in group Ator, whereas no significant difference of differentiation was found. CONCLUSION: Migration and survival of ASCs could be improved by atorvastatin under ischemia-reperfusion injury, which were ascribed to SDF-1α/CXCR-4 axis.


Assuntos
Tecido Adiposo/metabolismo , Movimento Celular/efeitos dos fármacos , Quimiocina CXCL12/metabolismo , Ácidos Heptanoicos/farmacologia , Inibidores de Hidroximetilglutaril-CoA Redutases/farmacologia , Transplante de Células-Tronco Mesenquimais , Células-Tronco Mesenquimais/metabolismo , Traumatismo por Reperfusão Miocárdica , Pirróis/farmacologia , Receptores CXCR4/metabolismo , Tecido Adiposo/patologia , Aloenxertos , Animais , Atorvastatina , Sobrevivência Celular/efeitos dos fármacos , Masculino , Células-Tronco Mesenquimais/patologia , Traumatismo por Reperfusão Miocárdica/metabolismo , Traumatismo por Reperfusão Miocárdica/patologia , Traumatismo por Reperfusão Miocárdica/terapia , Miócitos Cardíacos/metabolismo , Miócitos Cardíacos/patologia , Ratos , Ratos Sprague-Dawley
18.
Dis Markers ; 35(6): 857-62, 2013.
Artigo em Inglês | MEDLINE | ID: mdl-24367139

RESUMO

BACKGROUND AND AIM: Incidence of coronary restenosis after stent placement is high. Our study was going to investigate whether Lp(a) elevation was potential for predicting coronary restenosis and whether the effects of Lp(a) elevation on coronary restenosis were dependent on LDL-C level. METHODS AND RESULTS: Totally 832 participants eligible for stent placement were enrolled and followed up for monitoring clinical end points. Baseline characteristics were collected. According to the cut point of Lp(a), participants were divided into low Lp(a) group (Lp(a) < 30 mg/dL) and high Lp(a) group (Lp(a) ≥ 30 mg/dL). Furthermore, based on baseline LDL-C level, participants were divided into LDL-C < 1.8 mmol/L and ≥1.8 mmol/L subgroups. Clinical end points including major adverse cardiovascular events (MACE), cardiovascular death, nonfatal myocardial infarction, ischemic stroke, and coronary revascularization (CR) were compared. Patients in high Lp(a) groups more frequently presented with acute coronary syndrome and three vessel stenoses. In subgroup of LDL-C < 1.8 mmol/L, no significant differences of cardiovascular outcomes were found between low and high Lp(a) groups. While in the subgroup of LDL-C ≥ 1.8 mmol/L, incidences of MACE and CR were significantly higher in high Lp(a) group, and odds ratio for CR was 2.05. CONCLUSION: With baseline LDL-C and Lp(a) elevations, incidence of CR is significantly increased after stent placement.


Assuntos
LDL-Colesterol/sangue , Doença da Artéria Coronariana/sangue , Reestenose Coronária/sangue , Lipoproteína(a)/sangue , Neovascularização Patológica/sangue , Idoso , Doença da Artéria Coronariana/mortalidade , Doença da Artéria Coronariana/fisiopatologia , Doença da Artéria Coronariana/cirurgia , Progressão da Doença , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Neovascularização Patológica/mortalidade , Neovascularização Patológica/prevenção & controle , Risco , Stents , Resultado do Tratamento
19.
Dis Markers ; 35(5): 551-9, 2013.
Artigo em Inglês | MEDLINE | ID: mdl-24249942

RESUMO

Atherosclerotic cardiovascular diseases (CVD) are still the leading cause of morbidity and mortality worldwide, although optimal medical therapy has been prescribed for primary and secondary preventions. Residual cardiovascular risk for some population groups is still considerably high although target low density lipoprotein-cholesterol (LDL-C) level has been achieved. During the past few decades, compelling pieces of evidence from clinical trials and meta-analyses consistently illustrate that lipoprotein(a) (Lp(a)) is a significant risk factor for atherosclerosis and CVD due to its proatherogenic and prothrombotic features. However, the lack of effective medication for Lp(a) reduction significantly hampers randomized, prospective, and controlled trials conducting. Based on previous findings, for patients with LDL-C in normal range, Lp(a) may be a useful marker for identifying and evaluating the residual cardiovascular risk, and aggressively lowering LDL-C level than current guidelines' recommendation may be reasonable for patients with particularly high Lp(a) level.


Assuntos
Doença da Artéria Coronariana/diagnóstico , Lipoproteína(a)/metabolismo , Biomarcadores , LDL-Colesterol/sangue , Doença da Artéria Coronariana/sangue , Doença da Artéria Coronariana/metabolismo , Humanos , Lipoproteína(a)/sangue , Lipoproteína(a)/química , Medição de Risco
20.
BMC Med ; 11: 177, 2013 Aug 02.
Artigo em Inglês | MEDLINE | ID: mdl-23915102

RESUMO

BACKGROUND: Prospective cohort studies of prehypertension and the incidence of cardiovascular disease (CVD) are controversial after adjusting for other cardiovascular risk factors. This meta-analysis evaluated the association between prehypertension and CVD morbidity. METHODS: Databases (PubMed, EMBASE and the Cochrane Library) and conference proceedings were searched for prospective cohort studies with data on prehypertension and cardiovascular morbidity. Two independent reviewers assessed the reports and extracted data. The relative risks (RRs) of CVD, coronary heart disease (CHD) and stroke morbidity were calculated and reported with 95% confidence intervals (95% CIs). Subgroup analyses were conducted on blood pressure, age, gender, ethnicity, follow-up duration, number of participants and study quality. RESULTS: Pooled data included the results from 468,561 participants from 18 prospective cohort studies. Prehypertension elevated the risks of CVD (RR = 1.55; 95% CI = 1.41 to 1.71); CHD (RR = 1.50; 95% CI = 1.30 to 1.74); and stroke (RR = 1.71; 95% CI = 1.55 to 1.89). In the subgroup analyses, even for low-range prehypertension, the risk of CVD was significantly higher than for optimal BP (RR = 1.46, 95% CI = 1.32 to 1.62), and further increased with high-range prehypertension (RR = 1.80, 95% CI = 1.41 to 2.31). The relative risk was significantly higher in the high-range prehypertensive populations than in the low-range populations (χ2= 5.69, P = 0.02). There were no significant differences among the other subgroup analyses (P>0.05). CONCLUSIONS: Prehypertension, even in the low range, elevates the risk of CVD after adjusting for multiple cardiovascular risk factors.


Assuntos
Doenças Cardiovasculares/diagnóstico , Doenças Cardiovasculares/epidemiologia , Pré-Hipertensão/epidemiologia , Pressão Sanguínea/fisiologia , Doenças Cardiovasculares/fisiopatologia , Estudos de Coortes , Humanos , Hipertensão/diagnóstico , Hipertensão/epidemiologia , Hipertensão/fisiopatologia , Incidência , Pré-Hipertensão/diagnóstico , Pré-Hipertensão/fisiopatologia , Estudos Prospectivos
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