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1.
Nat Rev Cardiol ; 17(1): 52-63, 2020 01.
Artigo em Inglês | MEDLINE | ID: mdl-31366922

RESUMO

Flowing blood generates a frictional force called shear stress that has major effects on vascular function. Branches and bends of arteries are exposed to complex blood flow patterns that exert low or low oscillatory shear stress, a mechanical environment that promotes vascular dysfunction and atherosclerosis. Conversely, physiologically high shear stress is protective. Endothelial cells are critical sensors of shear stress but the mechanisms by which they decode complex shear stress environments to regulate physiological and pathophysiological responses remain incompletely understood. Several laboratories have advanced this field by integrating specialized shear-stress models with systems biology approaches, including transcriptome, methylome and proteome profiling and functional screening platforms, for unbiased identification of novel mechanosensitive signalling pathways in arteries. In this Review, we describe these studies, which reveal that shear stress regulates diverse processes and demonstrate that multiple pathways classically known to be involved in embryonic development, such as BMP-TGFß, WNT, Notch, HIF1α, TWIST1 and HOX family genes, are regulated by shear stress in arteries in adults. We propose that mechanical activation of these pathways evolved to orchestrate vascular development but also drives atherosclerosis in low shear stress regions of adult arteries.


Assuntos
Aterosclerose/genética , Endotélio Vascular/metabolismo , Regulação da Expressão Gênica no Desenvolvimento , Mecanotransdução Celular/genética , Animais , Aterosclerose/metabolismo , Aterosclerose/fisiopatologia , Endotélio Vascular/fisiopatologia , Predisposição Genética para Doença , Humanos , Neovascularização Fisiológica/genética , Fenótipo , Fluxo Sanguíneo Regional , Fatores de Risco , Estresse Mecânico , Remodelação Vascular/genética
2.
J Bone Miner Metab ; 38(1): 70-77, 2020 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-31420749

RESUMO

Fibroblast growth factor (FGF) 23 is a bone-derived hormone regulating serum inorganic phosphate (Pi) concentration. FGF23 is also involved in the development of chronic kidney disease (CKD)-mineral and bone disorder. Serum FGF23 concentration begins to increase early in the progression of CKD and can be remarkably high in hemodialysis patients with end-stage renal disease. It has been reported that high FGF23 concentration is a risk factor for cardiac dysfunction, atherosclerosis, infection or systemic inflammation in CKD patients. FGF23 was also shown to induce cardiac hypertrophy directly acting on cardiomyocytes. However, it is still controversial whether high FGF23 is causing cardiac dysfunction, atherosclerosis, infection or systemic inflammation in CKD patients. In the current study, we investigated whether FGF23 concentration is associated with cardiac dysfunction, atherosclerosis, infection or systemic inflammation in Japanese hemodialysis patients. We recruited 119 hemodialysis patients and examined the association between serum FGF23 concentration and several parameters concerning mineral metabolism, cardiac dysfunction, atherosclerosis, infection, and systemic inflammation. Serum FGF23 concentration was independently associated with serum calcium and Pi concentration (ß = 0.276, p < 0.001; ß = 0.689, p < 0.001). However, serum FGF23 concentration was not associated with parameters of cardiac dysfunction, atherosclerosis, infection, and systemic inflammation, either. Our results do not support the hypothesis that high FGF23 in dialysis patients is the cause of cardiac dysfunction, atherosclerosis, infection or systemic inflammation.


Assuntos
Aterosclerose/sangue , Aterosclerose/fisiopatologia , Fatores de Crescimento de Fibroblastos/sangue , Coração/fisiopatologia , Inflamação/sangue , Diálise Renal , Idoso , Aterosclerose/complicações , Feminino , Humanos , Inflamação/complicações , Modelos Logísticos , Masculino , Análise de Regressão
3.
Environ Health Perspect ; 127(11): 117003, 2019 11.
Artigo em Inglês | MEDLINE | ID: mdl-31724879

RESUMO

BACKGROUND: Atherosclerotic cardiovascular disease has become the leading cause of death worldwide, and environmental pollutants are increasingly recognized as risk factors for atherosclerosis. Liver X receptors (LXRs) play a central role in atherosclerosis; however, LXR activity of organic pollutants and associated potential risk of atherosclerosis have not yet been characterized. OBJECTIVES: This study aimed to explore whether LXR-antagonistic chemicals are present in indoor house dust and, if so, to characterize this activity in relation to changes in macrophages in vitro and cardiovascular disease indicators in vivo in an atherosclerosis ApoE-/- mouse model. METHODS: We used a His-LXRα-pull-down assay and a nontarget high-resolution mass spectrometry method to screen house dust collected from Chinese homes for LXRα- and LXRß-antagonist activity. A chemical identified in this manner was assessed for its ability to induce cholesterol efflux and foam cell formation in RAW264.7 macrophages, to down-regulate the expression of two LXR-dependent genes, ABCA1 and ABCG1, and finally to induce atherosclerotic lesions in vivo using an ApoE-/- mouse model. RESULTS: We identified the flame retardants triphenyl phosphate (TPHP) and 2-ethylhexyl diphenyl phosphate (EHDPP) in house dust samples and demonstrated their ability to antagonize LXRs. The potency of TPHP was similar to that of the LXR-antagonist SR9238. TPHP could also inhibit cholesterol efflux and promote foam cell formation in RAW264.7 macrophages and mouse peritoneal macrophages and significantly promoted atherosclerotic lesion formation in the ApoE-/- mouse model. CONCLUSIONS: We found LXR-antagonist chemicals in environmental samples of indoor dust from Chinese homes. One of the chemicals, TPHP, was able to promote the development of atherosclerotic lesions in the ApoE-/- mouse model. These results highlight the need to assess the LXR-antagonist activities of pollutants in future environmental management programs. https://doi.org/10.1289/EHP5039.


Assuntos
Poluentes Atmosféricos/efeitos adversos , Poluição do Ar em Ambientes Fechados/análise , Aterosclerose/fisiopatologia , Poeira/análise , Animais , Aterosclerose/induzido quimicamente , China , Receptores X do Fígado/metabolismo , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Camundongos Knockout para ApoE , Células RAW 264.7
4.
Yonsei Med J ; 60(11): 1036-1044, 2019 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-31637885

RESUMO

PURPOSE: This study aimed to investigate the effect of adipose-derived stem cell (ADSC) transplantation on atherosclerosis (AS) and its underlying mechanisms. MATERIALS AND METHODS: In our study, rat AS model was established, and ADSCs were isolated and cultured. Atherosclerotic plaque and pathological symptoms of thoracic aorta were measured by Oil Red O staining and Hematoxylin-Eosin staining, respectively. Total cholesterol (TC), triglyceride (TG), high-density lipoprotein cholesterol (HDL-C), and low-density lipoprotein cholesterol (LDL-C) levels were measured by an automatic biochemical analyzer. Expressions of vascular endothelial growth factor (VEGF), vascular cell adhesion molecule-1 (VCAM-1), intercellular adhesion molecule-1 (ICAM-1), aortic endothelin-1 (ET-1), interleukin-6 (IL-6), c-reactive protein (CRP), and tumor necrosis factor α (TNF-α) were measured by enzyme linked immunosorbent assay, VEGF, VCAM-1, ICAM-1, ET-1, respectively, and NF-κB p65 mRNA expressions were detected by quantitative real-time polymerase chain reaction. Protein expressions of VEGF, VCAM-1, ICAM-1, ET-1, NF-κB p65, p-NF-κB p65, and IκBα were measured by western blot. Moreover, NF-κB p65 expression was measured by immunofluorescence staining. RESULTS: ADSC transplantation alleviated the pathological symptoms of aortic AS. ADSC transplantation decreased the levels of TC, TG, and LDL-C and increased serum HDL-C level. Meanwhile, ADSC transplantation decreased the levels of IL-6, CRP, and TNF-α in AS rats. Moreover, the expressions of VEGF, ET-1, VCAM-1, and ICAM-1 were decreased by ADSC transplantation. ADSC transplantation inhibited phosphorylation of NF-κB p65 and promoted IκBα expression in AS rats. CONCLUSION: Our study demonstrated that ADSC transplantation could inhibit vascular inflammatory responses and endothelial dysfunction by suppressing NF-κB pathway in AS rats.


Assuntos
Tecido Adiposo/citologia , Aterosclerose/fisiopatologia , Aterosclerose/terapia , Endotélio Vascular/fisiopatologia , Inflamação/terapia , Transplante de Células-Tronco , Animais , Aorta/patologia , Aterosclerose/sangue , Citocinas/sangue , Modelos Animais de Doenças , Endotélio Vascular/patologia , Inflamação/sangue , Inflamação/patologia , Lipídeos/sangue , Masculino , Camundongos Endogâmicos C57BL , NF-kappa B/metabolismo , Ratos Sprague-Dawley , Transdução de Sinais
5.
Rev Cardiovasc Med ; 20(3): 121-128, 2019 Sep 30.
Artigo em Inglês | MEDLINE | ID: mdl-31601086

RESUMO

Recent studies have shown that the integrity of the gastrointestinal tract and its microbiome impact the functioning of various body systems by regulating immunological responses, extracting energy, remodeling intestinal epithelia, and strengthening the gut itself. The gastrointestinal tract microbiota includes bacteria, fungi, protozoa, viruses, and archaea which collectively comprise a dynamic community prone to alterations via influences such as the environment, illness, and metabolic processes. The idea that the host's diet possesses characteristics that could potentially alter microbiota composition is a novel notion. We hypothesize that a high fat diet leads to the alteration of the gastrointestinal microbiota composition and that metabolic transformation of the compound trimethylamine into trimethylamine-N-oxide promotes vasculopathy such as atherosclerosis and affects cardiovascular functionality. Furthermore, we hypothesize that treatment with probiotics will restore the homeostatic environment (eubiosis) of the gastrointestinal tract.


Assuntos
Aterosclerose/metabolismo , Bactérias/metabolismo , Dieta Hiperlipídica/efeitos adversos , Endotélio Vascular/metabolismo , Microbioma Gastrointestinal , Metilaminas/metabolismo , Animais , Aterosclerose/microbiologia , Aterosclerose/fisiopatologia , Aterosclerose/terapia , Bactérias/crescimento & desenvolvimento , Disbiose , Endotélio Vascular/fisiopatologia , Interações Hospedeiro-Patógeno , Humanos , Lipídeos/sangue , Placa Aterosclerótica , Probióticos/uso terapêutico , Fatores de Risco
6.
Isr Med Assoc J ; 21(7): 460-463, 2019 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-31507121

RESUMO

BACKGROUND: Inflammation is the basic mechanism leading to many pathological processes, including degenerative diseases, atherosclerosis, and cancer. We found an interesting link connecting rheumatoid arthritis and atherosclerosis that may explain the high cardiovascular event rate among patients with rheumatoid arthritis, but also may lead to a new way of thinking and a better understanding of atherosclerosis. Rheumatoid arthritis could serve as a model of accelerated atherosclerosis. Understanding the basic mechanisms of rheumatoid arthritis may solve some of the complexity of atherosclerosis.


Assuntos
Artrite Reumatoide/fisiopatologia , Aterosclerose/fisiopatologia , Inflamação/fisiopatologia , Doenças Cardiovasculares/epidemiologia , Doenças Cardiovasculares/fisiopatologia , Humanos , Fatores de Risco
8.
J Biomed Sci ; 26(1): 56, 2019 Aug 07.
Artigo em Inglês | MEDLINE | ID: mdl-31387590

RESUMO

BACKGROUND: Endothelial cell (EC) dysfunctions, including turnover enrichment, gap junction disruption, inflammation, and oxidation, play vital roles in the initiation of vascular disorders and atherosclerosis. Hemodynamic forces, i.e., atherprotective pulsatile (PS) and pro-atherogenic oscillatory shear stress (OS), can activate mechanotransduction to modulate EC function and dysfunction. This review summarizes current studies aiming to elucidate the roles of epigenetic factors, i.e., histone deacetylases (HDACs), non-coding RNAs, and DNA methyltransferases (DNMTs), in mechanotransduction to modulate hemodynamics-regulated EC function and dysfunction. OS enhances the expression and nuclear accumulation of class I and class II HDACs to induce EC dysfunction, i.e., proliferation, oxidation, and inflammation, whereas PS induces phosphorylation-dependent nuclear export of class II HDACs to inhibit EC dysfunction. PS induces overexpression of the class III HDAC Sirt1 to enhance nitric oxide (NO) production and prevent EC dysfunction. In addition, hemodynamic forces modulate the expression and acetylation of transcription factors, i.e., retinoic acid receptor α and krüppel-like factor-2, to transcriptionally regulate the expression of microRNAs (miRs). OS-modulated miRs, which stimulate proliferative, pro-inflammatory, and oxidative signaling, promote EC dysfunction, whereas PS-regulated miRs, which induce anti-proliferative, anti-inflammatory, and anti-oxidative signaling, inhibit EC dysfunction. PS also modulates the expression of long non-coding RNAs to influence EC function. i.e., turnover, aligmant, and migration. On the other hand, OS enhances the expression of DNMT-1 and -3a to induce EC dysfunction, i.e., proliferation, inflammation, and NO repression. CONCLUSION: Overall, epigenetic factors play vital roles in modulating hemodynamic-directed EC dysfunction and vascular disorders, i.e., atherosclerosis. Understanding the detailed mechanisms through which epigenetic factors regulate hemodynamics-directed EC dysfunction and vascular disorders can help us to elucidate the pathogenic mechanisms of atherosclerosis and develop potential therapeutic strategies for atherosclerosis treatment.


Assuntos
Aterosclerose/fisiopatologia , Células Endoteliais/fisiologia , Epigênese Genética , Animais , Aterosclerose/enzimologia , Aterosclerose/genética , Metilação de DNA/genética , Células Endoteliais/enzimologia , Células Endoteliais/patologia , Hemodinâmica , Histona Desacetilases/genética , Histona Desacetilases/metabolismo , Humanos , Mecanotransdução Celular/genética , RNA não Traduzido/genética , RNA não Traduzido/metabolismo
9.
Clín. investig. arterioscler. (Ed. impr.) ; 31(4): 152-159, jul.-ago. 2019. graf, tab
Artigo em Espanhol | IBECS | ID: ibc-182709

RESUMO

Introducción: La participación monocitaria en la progresión aterosclerótica y sus efectos pro- o antiinflamatorios dependen de las subpoblaciones circulantes. El objetivo de este estudio es la caracterización de dichas subpoblaciones y su asociación con los factores de riesgo cardiovascular. Métodos: Estudio transversal que incluye 102 pacientes seleccionados; edad media: 65 años (rango 41-86 años), 69% varones. Se utilizó un panel de anticuerpos específicos frente a monocitos clásicos (Mon1, CD14+CD16− CD300e+HLADR+), intermedios (Mon2, CD14+CD16+CD300e+HLADR+) y no clásicos (Mon3, CD14-k-CD16+CD300e+HLADR+). Se establecieron tres grupos de estudio; grupo 1: sujetos asintomáticos con más de un factor de riesgo cardiovascular (n = 17); grupo 2: sujetos asintomáticos, pero con patología vascular por ecografía o microalbuminuria (n = 56); y grupo 3: pacientes con algún evento vascular aterotrombótico previo (n = 19). Asimismo, se calculó el riesgo cardiovascular mediante las escalas Framingham y REGICOR. Resultados: Se observó una asociación entre las subpoblaciones Mon1 y Mon2 y los grupos del estudio (ANOVA, p < 0,05), independiente de la edad y el sexo para los Mon2. Asimismo, las subpoblaciones Mon1 y Mon 2 se asociaron con eventos vasculares adversos (ß = 0,86, p = 0,02 y ß = 0,1 p = 0,002, respectivamente), siendo la asociación de Mon2 independiente de la edad y el sexo. Además, el porcentaje de Mon3 se asoció con la presencia de más de 2 factores de riesgo cardiovascular (ß=0,21, p=0,04) en el análisis univariante. Finalmente, se halló una correlación entre los niveles de Mon1 y Mon2 con el número de leucocitos (r = 0,7, p < 0,001 y r = 0,26 p < 0,01, respectivamente). Conclusiones: El análisis de subpoblaciones monocitarias es de gran interés clínico, ya que permite establecer un diferente perfil inflamatorio según los grupos de riesgo cardiovascular establecidos


Introduction: Monocytes play an important role in atherosclerotic progression having both pro and anti-inflammatory effects depending on different circulating monocyte subpopulations. The objective of this study is to characterize these subpopulations and their association with cardiovascular risk factors. Methods: Transversal study including 102 selected patients, mean age: 65 years-old (range 41-86), 69% males. A set of specific antibodies against classical monocytes (Mon1, CD14+CD16- CD300e+HLADR+), intermediate (Mon2, CD14+CD16+CD300e+HLADR+) and non-classical (Mon3, CD14-CD16+CD300e+HLADR+) was assayed. Three groups of patients were included: 17 asymptomatic with more than one cardiovascular risk factor (group 1), 56 subjects asymptomatic but with vascular pathology assessed by ultrasound or microalbuminuria (group 2) and 19 patients with a previous atherothrombotic event (group 3). The cardiovascular risk was determined by Framingham and REGICOR scores. Results: An association between study groups and the percentage of Mon1 and Mon2 was observed (ANOVA, p < .05), being independent of age and sex for Mon2. Likewise Mon1 and Mon2 subpopulations were associated with cardiovascular adverse events (ß = 0.86, p =.02 y ß = 0.1 p =.002, respectively), independently of age and sex in the case of Mon2. Moreover the percentage of Mon3 was associated with the presence of several cardiovascular risk factors (ß = 0.21, p = .04) in the univariate analysis. In addition, there was a correlation between the levels of Mon1 and Mon2 and leukocytes (r = 0.7, p < .001 and r = 0.26, p = .01, respectively). Conclusions: The analysis of monocyte subpopulations may be clinically useful to stratify the inflammatory profile related to the different cardiovascular risk groups


Assuntos
Humanos , Masculino , Adulto , Pessoa de Meia-Idade , Idoso , Idoso de 80 Anos ou mais , Monócitos , Fatores de Risco , Doenças Cardiovasculares/diagnóstico , Aterosclerose/complicações , Estudos Transversais , Análise de Variância , Aterosclerose/diagnóstico , Aterosclerose/fisiopatologia , Grupos de Risco
10.
Curr Med Sci ; 39(4): 513-522, 2019 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-31346984

RESUMO

Necroptosis is a non-apoptotic programmed cell death pathway, which causes necrosis-like morphologic changes and triggers inflammation in the surrounding tissues. Accumulating evidence has demonstrated that necroptosis is involved in a number of pathological processes that lead to cardiovascular diseases. However, the exact molecular pathways linking them remain unknown. Herein, this review summarizes the necroptosis-related pathways involved in the development of various cardiovascular diseases, including atherosclerosis, cardiac ischemia-reperfusion injury, cardiac hypertrophy, dilated cardiomyopathy and myocardial infarction, and may shed light on the diagnosis and treatment of these diseases.


Assuntos
Apoptose/genética , Doenças Cardiovasculares/genética , Morte Celular/genética , /genética , Aterosclerose/genética , Aterosclerose/fisiopatologia , Cardiomegalia/genética , Cardiomegalia/fisiopatologia , Cardiomiopatia Dilatada/genética , Cardiomiopatia Dilatada/fisiopatologia , Doenças Cardiovasculares/fisiopatologia , Humanos , Infarto do Miocárdio/genética , Infarto do Miocárdio/fisiopatologia , Traumatismo por Reperfusão/genética , Traumatismo por Reperfusão/fisiopatologia , Transdução de Sinais/genética
11.
Complement Ther Med ; 45: 211-214, 2019 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-31331563

RESUMO

BACKGROUND: Individuals diagnosed with congestive heart failure (CHF) have a 50% five-year mortality rate and approximately 650,000 new cases of CHF are diagnosed annually. Plant-based diets are known to improve plasma lipid concentrations, reduce blood pressure, and as part of a lifestyle intervention, lead to the regression of atherosclerotic lesions. However, a paucity of data exists with regards to plant-based diets in the treatment of CHF. METHODS: Three patients diagnosed with CHF opted to undergo a dietary intervention consisting of a defined plant-based diet as an adjunct to standard medical treatment for CHF. Cardiac magnetic resonance imaging was performed. Patients' consumed the defined plant-based diet for an average of ˜79 days. RESULTS: Follow-up cardiac magnetic resonance images revealed a 92% increase in ejection fraction [mean ±â€¯standard deviation for all data] (22.0 ±â€¯6.9% vs 42.2 ±â€¯18.4%), 21% reduction in left ventricular mass (214 ±â€¯90 g vs 170 ±â€¯102 g), 62% increase in stroke volume (55.8 ±â€¯24.3 cc vs 90.3 ±â€¯30.6 cc) and a 17% increase in cardiac output (3.6 ±â€¯1.2 L/min vs 4.2 ±â€¯1.6 L/min). In patient 1, 90-95% ostial stenosis of the left anterior descending artery nearly completely regressed following the dietary intervention. All patients subjectively reported significant clinical improvements, including less angina, shortness of breath and fatigue. CONCLUSION: As an adjunct treatment, a defined plant-based diet may contribute to the reversal of cardiac morphological and functional abnormalities in the setting of CHF.


Assuntos
Insuficiência Cardíaca/dietoterapia , Idoso , Aterosclerose/fisiopatologia , Pressão Sanguínea/fisiologia , Débito Cardíaco/fisiologia , Dieta Vegetariana , Feminino , Ventrículos do Coração/fisiopatologia , Humanos , Masculino , Pessoa de Meia-Idade , Volume Sistólico/fisiologia
12.
Neoplasma ; 66(6): 978-987, 2019 11.
Artigo em Inglês | MEDLINE | ID: mdl-31305124

RESUMO

Long-term survivors of Hodgkin lymphoma during childhood or adolescence (HL survivors) are at high risk of developing treatment-related late cardiovascular sequelae. In our study we evaluated the presence of modifiable cardiovascular risk factors (hypertension, hyperlipoproteinemia, hyperinsulinemia, obesity), endothelial and inflammatory markers (E-selectin, PAI-1, hs-CRP) and atherosclerotic changes in the common carotid arteries. Assessment was performed in 80 young adult Hodgkin lymphoma long-term survivors at more than 10 years after the potentially cardiovascular toxic anticancer treatment (median age at evaluation 34.7 years; range 24.1-40.9 years). The HL survivors were compared with 83 age- and gender-matched healthy volunteers. The HL survivors showed unfavorable lipid profiles compared to those of healthy controls: triglycerides (p=0.01), total cholesterol (p=0.0004), low density lipoprotein cholesterol (p=0.005). In HL survivors, we found a higher prevalence of hypertension (p=0.004) and insulin resistance - HOMA-IR (p=0.0002). Ultrasonographic examination of both common carotid arteries revealed a higher prevalence of atherosclerotic plaques (p=0.0009) and higher carotid intima-media thickness (p<0.0001) in HL survivors. Markers of oxidative stress (advanced oxidation protein products, oxidized low-density lipoprotein), inflammation (hs-CRP) and endothelial dysfunction (E-selectin, PAI-1) were also higher in HL survivors (p<0.0001, p=0.0002, p=0.0031, p=0.0087, p=0.004, respectively). Adult survivors of Hodgkin lymphoma during childhood and adolescence need closer follow-up with screening of metabolic syndrome components, unfavorable lifestyle factors and early management of these risk factors.


Assuntos
Aterosclerose , Doença de Hodgkin , Hiperlipoproteinemias , Resistência à Insulina , Adolescente , Adulto , Aterosclerose/etiologia , Aterosclerose/fisiopatologia , Espessura Intima-Media Carotídea , Criança , Doença de Hodgkin/complicações , Humanos , Hiperlipoproteinemias/etiologia , Hiperlipoproteinemias/fisiopatologia , Sobreviventes , Adulto Jovem
13.
Acta Otolaryngol ; 139(9): 793-797, 2019 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-31268381

RESUMO

Background: Obstructive sleep apnea (OSA) is associated with several cardiovascular comorbidities including hypertension, arteriosclerosis, and heart failure. Uvulopalatopharyngoplasty (UPPP) is a frequently performed surgical treatment for OSA. Aims/Objectives: To analyze if UPPP can improve cardiac parameters associated with atherosclerosis and reduce the cardiac burden in OSA patients. Material and methods: A prospective cohort study was performed at a single tertiary care center where OSA patients undergoing UPPP were evaluated. Preoperative and 6-month postoperative cardiac parameters namely carotid artery intima-media thickness (CIMT), arterial stiffness parameters, echocardiography, and polysomnography (PSG) results were compared. Results: Fifty three patients were included in the study. The success and response rate of UPPP was 60.4%. Following the surgery, significant reduction in arterial stiffness index (ß) (12.4 ± 4.1 vs. 11.2 ± 4.0, p = .01), and elasticity modulus (Ep) (172.8 ± 68.3 vs. 156.6 ± 55.3, p = .05) was noticed. Additionally, echocardiographic parameters namely velocity across aortic valve (121.9 ± 22.9 vs. 109.4 ± 17.7, p = .01) and velocity across pulmonary valve (107.4 ± 16.4 vs. 94.2 ± 16.9, p < .01) significantly decreased following UPPP. Conclusions and significance: UPPP significantly improves parameters related to carotid atherosclerosis and has the potential to reduce cardiac burden in OSA patients.


Assuntos
Aterosclerose/epidemiologia , Doenças Cardiovasculares/epidemiologia , Procedimentos Cirúrgicos Reconstrutivos/métodos , Apneia Obstrutiva do Sono/epidemiologia , Apneia Obstrutiva do Sono/cirurgia , Úvula/cirurgia , Adulto , Aterosclerose/fisiopatologia , Doenças Cardiovasculares/diagnóstico , Espessura Intima-Media Carotídea , Estudos de Coortes , Comorbidade , Feminino , Seguimentos , Humanos , Masculino , Pessoa de Meia-Idade , Palato Mole/cirurgia , Faringe/cirurgia , Polissonografia/métodos , Estudos Prospectivos , Medição de Risco , Apneia Obstrutiva do Sono/diagnóstico , Centros de Atenção Terciária , Resultado do Tratamento
14.
Clin Interv Aging ; 14: 789-796, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31190766

RESUMO

Objective: Ageing is one of the major risks for atherosclerosis. The age-related changes of interactions between plasma lipids, oxidative stress, antioxidant defense, and glycation processes are still not established while we age. Thus, the aim of the study was to analyze such relationships in individuals at risk for atherosclerosis due to their age. Methods: Elderly and middle-aged persons with no acute disease or severe chronic disorder were assessed. Fasting plasma lipids (total cholesterol (T-C), high-density lipoprotein-cholesterol (HDL-C), low-density lipoprotein-cholesterol, and triacylglycerols), thiobarbituric acid reacting substances (TBARS), plasma total antioxidant status (TAS), and glucose and glycated proteins (fructosamine (FA) and glycated hemoglobin (HbA1c)) were determined. An oral glucose tolerance test allowed exclusion of persons with type 2 diabetes. Results: Lipid profiles were significantly profitable, increased HDL-C especially (p<0.0001), in the elderly versus middle-aged group. Decreased TBARS and TAS were found in the elderly versus middle-aged group (p=0.0001 and p=0.00002, respectively). Increased fructosamine was found in the elderly (255±30 µmol/L) versus middle-aged (236±33 µmol/L) group (p=0.006). Multiple regression analysis showed that in the middle-aged group TBARS correlated with T-C and HDL-C, and in the elderly group with HbA1c and FA independently of other factors. Conclusion: The factors which have an impact on oxidant-antioxidant status are crucial to understanding the pathomechanisms of senescence as well as the development of chronic diseases. Healthy aging may be maintained throughout proper lipid control. Moreover, data support the premise that the balance between lipid metabolism and oxidative stress may play a role in the initial phases of glycation plasma proteins particularly among elderly persons.


Assuntos
Antioxidantes/análise , Aterosclerose/epidemiologia , Aterosclerose/fisiopatologia , Hemoglobina A Glicada/análise , Lipídeos/sangue , Idoso , Envelhecimento/fisiologia , Antioxidantes/metabolismo , Glicemia/metabolismo , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Substâncias Reativas com Ácido Tiobarbitúrico/análise
15.
Clin Interv Aging ; 14: 849-857, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31190771

RESUMO

Purpose: Age-related reduction in bone marrow activity has been shown to cause anemia, and hypertension and endothelial dysfunction (atherosclerosis) are age-related diseases. However, recent studies have revealed a close association between bone marrow activity and endothelial maintenance. This study aimed to determine the association between elevated reticulocyte levels in conjunction with vigorous bone marrow activity and hypertension and atherosclerosis among the elderly. Study population and Methods: To determine the associations between reticulocyte levels and hypertension and atherosclerosis, we conducted a cross-sectional study of 2,098 elderly Japanese individuals, aged between 60 and 89 years, who had participated in an annual health check-up in 2014. Results: Of the total study population, 1,348 individuals were diagnosed with hypertension (systolic blood pressure ≥140 mmHg and/or diastolic blood pressure ≥90 mmHg and/or having used antihypertensive medication), and 393 were diagnosed with atherosclerosis (carotid intima-media thickness ≥1.1 mm). Reticulocyte levels were found to be significantly positively associated with hypertension and inversely associated with atherosclerosis. Cardiovascular risk factor-adjusted odds ratios and 95% confidence intervals for hypertension and atherosclerosis, when raised incrementally by 1 standard deviation to determine reticulocyte levels (5.5×104 cells/µL for men and 5.0×104 cells/µL for women), were 1.12 (1.01, 1.25) and 0.83 (0.72, 0.94), respectively. Conclusion: Along with established cardiovascular risk factors, reticulocyte levels in elderly Japanese individuals were found to be positively associated with hypertension and inversely associated with atherosclerosis. This finding may help clarify the background mechanisms concerning the association between bone marrow activity and vascular remodeling.


Assuntos
Aterosclerose/epidemiologia , Hipertensão/epidemiologia , Reticulócitos/metabolismo , Idoso , Idoso de 80 Anos ou mais , Aterosclerose/fisiopatologia , Pressão Sanguínea , Estudos Transversais , Feminino , Humanos , Hipertensão/fisiopatologia , Japão/epidemiologia , Masculino , Pessoa de Meia-Idade , Razão de Chances
16.
BMC Res Notes ; 12(1): 336, 2019 Jun 13.
Artigo em Inglês | MEDLINE | ID: mdl-31196144

RESUMO

OBJECTIVE: The study was dedicated to investigation of some hemostasis and endothelial dysfunction factors association with probability of presence of vulnerable atherosclerotic plaques in coronary arteries in men with atherosclerosis. RESULTS: The blood levels of factor VII, factor XII and MCP-1 were higher, and concentration of sVCAM-1 lower in men with vulnerable atherosclerotic plaques in the coronary arteries, compared to men who had stable plaques. Have been revealed correlation links between the blood levels of factor II, factor XII, MCP-1 and the presence of vulnerable atherosclerotic plaques in the coronary arteries. Results of logistic regression analysis showed that the relative risk of present of vulnerable atherosclerotic plaques in the coronary arteries is associated with an elevated blood level of factor XII and MCP-1.


Assuntos
Aterosclerose/fisiopatologia , Doença da Artéria Coronariana/fisiopatologia , Endotélio Vascular/fisiopatologia , Hemostasia , Placa Aterosclerótica/fisiopatologia , Idoso , Aterosclerose/sangue , Quimiocina CCL2/sangue , Doença da Artéria Coronariana/sangue , Vasos Coronários/metabolismo , Vasos Coronários/fisiopatologia , Endotélio Vascular/metabolismo , Fator XII/metabolismo , Humanos , Modelos Logísticos , Masculino , Pessoa de Meia-Idade , Placa Aterosclerótica/sangue , Probabilidade , Protrombina/metabolismo , Molécula 1 de Adesão de Célula Vascular/sangue
17.
Appl Microbiol Biotechnol ; 103(15): 5993-6006, 2019 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-31201452

RESUMO

Atherosclerosis is the major cause of cardiovascular diseases, which are considered the fatal ailment globally. Hypercholesterolaemia plays a critical role in the development of atherosclerosis and cardiovascular diseases. Many studies have been stated that probiotics could affect hypercholesterolemia via cholesterol metabolism. Probiotics are live bacteria which are good for our health when administered orally in high amounts. Recently, many studies have revealed the beneficial effects of the nutritional ingestion of probiotics which can decrease serum cholesterol levels. The aim of this review is, firstly, to explore the hypercholesterolemia effect of how it progresses into atherosclerosis and, secondly, to summarize the hypocholesterolaemia effect of probiotics on atherosclerosis and the up-to-date information on their basic mechanisms. The most important mechanisms responsible for the hypocholesterolemic effect of probiotics are the suppression of the reabsorption of bile acids and inhibition of the intestinal cholesterol absorption. Current studies indicate that numerous mechanisms within the cholesterol metabolism, e.g., ones involving the Niemann-Pick C1-Like 1 protein, 3-hydroxy-3-methylglutaryl-CoA reductase, and 7α- and 27α-hydroxylases, have been recommended where regulation may take place after oral intake of probiotics. However, these mechanisms are still poorly understood. Thus, further studies are required to examine the possible mechanisms, whereby probiotics can be utilized safely and considered for the treatment of hypercholesterolemia.


Assuntos
Aterosclerose/prevenção & controle , Aterosclerose/fisiopatologia , Hipercolesterolemia/complicações , Hipercolesterolemia/terapia , Probióticos/administração & dosagem , Probióticos/farmacologia , Animais , Colesterol/metabolismo , Humanos
18.
Turk Kardiyol Dern Ars ; 47(4): 251-257, 2019 Jun.
Artigo em Turco | MEDLINE | ID: mdl-31219439

RESUMO

OBJECTIVE: The pathophysiology of the slow coronary flow (SCF) phenomenon is still unclear. The two most frequently cited mechanisms of SCF are endothelial dysfunction and subclinical diffuse atherosclerosis. The aim of this study was to investigate the relation of SCF to serum endocan levels which is associated with endothelial dysfunction and to serum omentin-I levels which is associated with atherosclerosis. METHODS: A total of 42 patients with SCF and 43 controls with normal coronary flow based on a coronary angiogram were enrolled. Serum endocan and omentin-I levels were measured and the presence of SCF was determined according to Thrombolysis in Myocardial Infarction frame count (TFC) calculations. RESULTS: The omentin-I level was significantly lower and the endocan level was significantly higher in patients with SCF than in the controls. Receiver operating characteristic curve analysis revealed that the sensitivity and specificity of endocan for SCF was 66% and 70%, respectively (area under the curve [AUC]: 0.760, 95% confidence interval [CI]: 0.65-0.86; p<0.001), and the comparable values for omentin were 66% and 61% (AUC: 0.630, 95% CI: 0.51-0.75; p=0.049). Multivariate logistic regression analysis revealed that a high endocan level (odds ratio [OR]: 6.8, 95% CI: 1.849-2.439, cutoff: 2.45 ng/mL; p=0.003) and a low omentin-I level (OR: 3.6, 95% CI: 1.057-12.893, cutoff: 4.63 ng/mL; p=0.041) were independently associated with the presence of SCF. In patients with SCF, the endocan level was positively correlated with the mean TFC, while the omentin-I level was negatively correlated (r=0.44; p<0.001 and r=-0.22; p=0.049, respectively). CONCLUSION: These results revealed that endocan and omentin-I might be useful biomarkers for predicting the presence and severity of SCF.


Assuntos
Aterosclerose/fisiopatologia , Doença da Artéria Coronariana/fisiopatologia , Circulação Coronária/fisiologia , Citocinas/sangue , Lectinas/sangue , Proteínas de Neoplasias/sangue , Proteoglicanas/sangue , Biomarcadores/sangue , Estudos de Casos e Controles , Angiografia Coronária , Proteínas Ligadas por GPI/sangue , Humanos , Masculino , Pessoa de Meia-Idade , Sensibilidade e Especificidade
19.
Int J Cardiovasc Imaging ; 35(10): 1903-1911, 2019 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-31209684

RESUMO

Familial hypercholesterolemia (FH) is an autosomal dominant disorder that affects 1 in 250 people. Aortic stiffness, measured by pulse wave velocity (PWV), is an independent predictor for cardiovascular events. Young FH patients are a unique group with early vessel wall disease that may serve to elucidate the determinants of aortic stiffness. We hypothesized that young FH patients would have early changes in aortic stiffness compared to healthy, age- and sex-matched reference values. Thirty-three FH patients ( ≥ 7 years age; mean age 14.6 ± 3.3 years; 26/33 on statin therapy) underwent cardiac MRI. PWV was determined using propagation of flow waveform from aortic arch phase contrast images. Distensibility and aortic wall thickness (AWT) were measured at the ascending, proximal descending, and diaphragmatic aorta. Ventricular volumes and left ventricular (LV) myocardial mass were measured from 2D cine images. These parameters were compared to age- and sex-matched reference values. FH patients had significantly higher PWV (4.5 ± 0.8 vs. 3.5 ± 0.3 m/s; p < 0.001), aortic distensibility, and ascending aortic wall thickness (1.37 ± 0.18 vs. 1.30 ± 0.02 mm; p < 0.05) compared to reference. There was no difference in aortic area or descending aortic wall thickness between groups. Young FH patients had aortic changes with increased aortic pulse wave velocity in the setting of increased aortic distensibility, accompanied by increased thickness of the ascending aortic wall. Presence of these early findings in young patients despite the majority being on statin therapy support enhanced screening and aggressive treatment of familial hypercholesterolemia to prevent potential future cardiovascular events.


Assuntos
Aorta/diagnóstico por imagem , Doenças da Aorta/diagnóstico por imagem , Aterosclerose/diagnóstico por imagem , Hiperlipoproteinemia Tipo II/complicações , Imagem Cinética por Ressonância Magnética , Análise de Onda de Pulso , Rigidez Vascular , Adolescente , Fatores Etários , Aorta/fisiopatologia , Doenças da Aorta/etiologia , Doenças da Aorta/fisiopatologia , Doenças da Aorta/prevenção & controle , Aterosclerose/etiologia , Aterosclerose/fisiopatologia , Aterosclerose/prevenção & controle , Estudos de Casos e Controles , Criança , Estudos Transversais , Progressão da Doença , Feminino , Predisposição Genética para Doença , Heterozigoto , Humanos , Inibidores de Hidroximetilglutaril-CoA Redutases/uso terapêutico , Hiperlipoproteinemia Tipo II/diagnóstico , Hiperlipoproteinemia Tipo II/tratamento farmacológico , Hiperlipoproteinemia Tipo II/genética , Masculino , Fenótipo , Placa Aterosclerótica , Valor Preditivo dos Testes , Estudos Prospectivos , Fatores de Risco , Remodelação Vascular
20.
Braz J Med Biol Res ; 52(5): e8108, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31038578

RESUMO

Animal models of diseases are invaluable tools of modern medicine. More than forty years have passed since the first successful experiments and the spectrum of available models, as well as the list of methods for creating them, have expanded dramatically. The major step forward in creating specific disease models was the development of gene editing techniques, which allowed for targeted modification of the animal's genome. In this review, we discuss the available tools for creating transgenic animal models, such as transgenesis methods, recombinases, and nucleases, including zinc finger nuclease (ZFN), transcription activator-like effector nuclease (TALEN), and CRISPR/Cas9 systems. We then focus specifically on the models of atherosclerosis, especially mouse models that greatly contributed to improving our understanding of the disease pathogenesis and we outline their characteristics and limitations.


Assuntos
Animais Geneticamente Modificados , Aterosclerose/fisiopatologia , Modelos Animais de Doenças , Engenharia Genética/métodos , Nucleases dos Efetores Semelhantes a Ativadores de Transcrição/metabolismo , Animais , Aterosclerose/genética , Pesquisa Biomédica/métodos , Feminino , Técnicas de Transferência de Genes , Humanos , Masculino , Camundongos
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