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1.
Int J Mol Sci ; 22(15)2021 Jul 30.
Artigo em Inglês | MEDLINE | ID: mdl-34360964

RESUMO

GPR39, a member of the ghrelin family of G protein-coupled receptors, is zinc-responsive and contributes to the regulation of diverse neurovascular and neurologic functions. Accumulating evidence suggests a role as a homeostatic regulator of neuronal excitability, vascular tone, and the immune response. We review GPR39 structure, function, and signaling, including constitutive activity and biased signaling, and summarize its expression pattern in the central nervous system. We further discuss its recognized role in neurovascular, neurological, and neuropsychiatric disorders.


Assuntos
Doenças Cardiovasculares/genética , Doenças do Sistema Nervoso/genética , Acoplamento Neurovascular , Receptores Acoplados a Proteínas G/metabolismo , Animais , Doenças Cardiovasculares/metabolismo , Doenças Cardiovasculares/fisiopatologia , Homeostase , Humanos , Doenças do Sistema Nervoso/metabolismo , Doenças do Sistema Nervoso/fisiopatologia , Receptores Acoplados a Proteínas G/genética , Transdução de Sinais
2.
Molecules ; 26(16)2021 Aug 17.
Artigo em Inglês | MEDLINE | ID: mdl-34443563

RESUMO

Paeonol is a naturally existing bioactive compound found in the root bark of Paeonia suffruticosa and it is traditionally used in Chinese medicine for the prevention and management of cardiovascular diseases. To date, a great deal of studies has been reported on the pharmacological effects of paeonol and its mechanisms of action in various diseases and conditions. In this review, the underlying mechanism of action of paeonol in cardiovascular disease has been elucidated. Recent studies have revealed that paeonol treatment improved endothelium injury, demoted inflammation, ameliorated oxidative stress, suppressed vascular smooth muscle cell proliferation, and repressed platelet activation. Paeonol has been reported to effectively protect the cardiovascular system either employed alone or in combination with other traditional medicines, thus, signifying it could be a hypothetically alternative or complementary atherosclerosis treatment. This review summarizes the biological and pharmacological activities of paeonol in the treatment of cardiovascular diseases and its associated underlying mechanisms for a better insight for future clinical practices.


Assuntos
Acetofenonas/farmacologia , Doenças Cardiovasculares/tratamento farmacológico , Acetofenonas/uso terapêutico , Animais , Doenças Cardiovasculares/metabolismo , Doenças Cardiovasculares/patologia , Doenças Cardiovasculares/fisiopatologia , Humanos
3.
Medicine (Baltimore) ; 100(31): e26861, 2021 Aug 06.
Artigo em Inglês | MEDLINE | ID: mdl-34397862

RESUMO

ABSTRACT: Cardiac rehabilitation (CR) can improve clinical indicators in patients with cardiovascular diseases. The literature reports a 20% reduction in all-cause mortality and a 27% reduction in heart-disease mortality following CR. Although its clinical efficacy has been established, there is uncertainty whether center-based (CBCR) is more effective than home-based (HBCR) programs in acute and subacute phases. We aimed to verify significant differences in their effectiveness for the improvement of cardiopulmonary function by analyzing cardiopulmonary exercise (CPX) with laboratory tests following both CR programs.A single-center cohort study of 37 patients, recently diagnosed with underlying cardiovascular diseases, underwent CBCR(18) and HBCR(19). CBCR group performed a supervised exercise regimen at the CR center, for 1 hour, 2 to 3 days a week, for a total of 12 to18 weeks. HBCR group completed a self-monitored exercise program at home under the same guidelines as CBCR. Participants were evaluated by CPX with laboratory tests at 1- and 6-month, following the respective programs.There was no statistical significance in clinical characteristics and laboratory findings. Pre-post treatment comparison showed significant improvement in VO2/kg, minute ventilation/carbon dioxide production slope, breathing reserve, tidal volume (VT), heart rate recovery, oxygen consumption per heart rate, low-density lipoprotein (LDL), LDL/HDL ratio, total cholesterol, ejection fraction (EF) (P < .05). CBCR approach showed greater improvement with significance in VO2/kg, metabolic equivalents, and EF on between groups analysis (P < .05).The time effect of CPX test and laboratory data showed improvement in cardiopulmonary function and serum indicators for both groups. VO2/kg, metabolic equivalents, and EF were among the variables that showed significant differences between groups. In the acute and subacute phases of 1 to 6 months, the CBCR group showed a greater cardiac output improvement than the HBCR group.


Assuntos
Biomarcadores/sangue , Reabilitação Cardíaca , Doenças Cardiovasculares , Terapia por Exercício , Serviços de Assistência Domiciliar/estatística & dados numéricos , Centros de Reabilitação/estatística & dados numéricos , Reabilitação Cardíaca/métodos , Reabilitação Cardíaca/normas , Doenças Cardiovasculares/sangue , Doenças Cardiovasculares/diagnóstico , Doenças Cardiovasculares/fisiopatologia , Doenças Cardiovasculares/terapia , Pesquisa Comparativa da Efetividade , Teste de Esforço/métodos , Terapia por Exercício/métodos , Terapia por Exercício/organização & administração , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Avaliação de Processos e Resultados em Cuidados de Saúde , República da Coreia/epidemiologia , Testes de Função Respiratória/métodos , Testes de Função Respiratória/estatística & dados numéricos , Resultado do Tratamento
4.
Medicine (Baltimore) ; 100(34): e26857, 2021 Aug 27.
Artigo em Inglês | MEDLINE | ID: mdl-34449455

RESUMO

ABSTRACT: The current global health crisis due to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has prompted the medical community to investigate the effects of underlying medical conditions, including sleep-disordered breathing, on inpatient care. Obstructive sleep apnea (OSA) is a common form of sleep-disordered breathing that may complicate numerous acquired conditions, particularly in inpatient and critical care settings. Viral pneumonia is a major contributor to intensive care unit (ICU) admissions and often presents more severely in patients with underlying pulmonary disease, especially those with obesity and OSA. This review summarizes the most recent data regarding complications of both OSA and obesity and highlights their impact on clinical outcomes in hospitalized patients. Additionally, it will highlight pertinent evidence for the complications of OSA in an organ-systems approach. Finally, this review will also discuss impatient treatment approaches for OSA, particularly in relation to the SARS-CoV-2 pandemic.


Assuntos
COVID-19/epidemiologia , Obesidade/epidemiologia , Apneia Obstrutiva do Sono/epidemiologia , Apneia Obstrutiva do Sono/fisiopatologia , COVID-19/fisiopatologia , Doenças Cardiovasculares/epidemiologia , Doenças Cardiovasculares/fisiopatologia , Humanos , Unidades de Terapia Intensiva , Obesidade/fisiopatologia , Infecções Respiratórias/epidemiologia , Infecções Respiratórias/fisiopatologia , Fatores de Risco , SARS-CoV-2 , Índice de Gravidade de Doença , Sonolência
5.
Medicine (Baltimore) ; 100(34): e27048, 2021 Aug 27.
Artigo em Inglês | MEDLINE | ID: mdl-34449492

RESUMO

ABSTRACT: Synchronous non-alcoholic fatty liver disease (NAFLD) and carotid artery plaque formation increase the risk of mortality in patients with cardiovascular disease (CVD). Metabolic status and host gut flora are associated with NAFLD and CVD, but the risk factors require further evaluation.To evaluate the risk factors associated with NAFLD and CVD, including gut-flora-related examinations.This cross-sectional study included 235 subjects aged over 40 years who underwent abdominal ultrasound examination and carotid artery ultrasound examination on the same day or within 12 months of abdominal ultrasound between January 2018 and December 2019. All subjects underwent blood tests, including endotoxin and trimethylamine-N-oxide.The synchronous NAFLD and carotid artery plaque subjects had a higher proportion of men and increased age compared with those without NAFLD and no carotid artery plaque. The synchronous NAFLD and carotid artery plaque group had increased body mass index (BMI), blood pressure, hemoglobin A1C (5.71% vs 5.42%), triglyceride (TG) (164.61 mg/dL vs 102.61 mg/dL), and low-density lipoprotein (135.27 mg/dL vs 121.42 mg/dL). In multiple logistic regression analysis, increased BMI, mean systolic blood pressure, and TG > 110 mg/dL were independent risk factors for synchronous NAFLD and carotid artery plaque formation. Endotoxin and trimethylamine-N-oxide levels were not significantly different between the 2 groups.Host metabolic status, such as elevated BMI, TG, and systolic blood pressure, are associated with synchronous NAFLD and carotid artery plaque in asymptomatic adults. Aggressive TG control, blood pressure control, and weight reduction are indicated in patients with NAFLD.


Assuntos
Estenose das Carótidas/epidemiologia , Estenose das Carótidas/fisiopatologia , Microbioma Gastrointestinal/fisiologia , Hepatopatia Gordurosa não Alcoólica/epidemiologia , Hepatopatia Gordurosa não Alcoólica/fisiopatologia , Adulto , Fatores Etários , Pressão Sanguínea , Índice de Massa Corporal , Doenças Cardiovasculares/epidemiologia , Doenças Cardiovasculares/fisiopatologia , Estudos Transversais , Hemoglobina A Glicada , Humanos , Lipídeos/sangue , Pessoa de Meia-Idade , Fatores Sexuais
6.
Molecules ; 26(16)2021 Aug 10.
Artigo em Inglês | MEDLINE | ID: mdl-34443410

RESUMO

Glucagon-like peptide-1 receptor agonists (GLP-1 RAs) are considered the standard of care for type 2 diabetes in many countries worldwide. These molecules have profound anti-hyperglycaemic actions with a favourable safety profile. They are now being considered for their robust cardiovascular (CV) protective qualities in diabetic patients. Most recent CV outcome trials have reported that GLP-1 RAs reduce major adverse cardiovascular events (MACE). Furthermore, the GLP-1 RAs seem to target the atherosclerotic CV disease processes preferentially. GLP-1 RAs also improve a wide range of routinely measured surrogate markers associated with CV risk. However, mediation analysis suggests these modest improvements may contribute indirectly to the overall anti-atherogenic profile of the molecules but fall short in accounting for the significant reduction in MACE. This review explores the body of literature to understand the possible mechanisms that contribute to the CV protective profile of GLP-1 RAs.


Assuntos
Doenças Cardiovasculares/tratamento farmacológico , Receptor do Peptídeo Semelhante ao Glucagon 1/agonistas , Animais , Pressão Sanguínea , Doenças Cardiovasculares/sangue , Doenças Cardiovasculares/imunologia , Doenças Cardiovasculares/fisiopatologia , Humanos , Imunidade , Mitocôndrias Cardíacas/metabolismo , Comportamento de Redução do Risco
7.
Nutrients ; 13(7)2021 Jul 10.
Artigo em Inglês | MEDLINE | ID: mdl-34371871

RESUMO

Coronary Heart Disease (CHD) is a major mortality and morbidity cause in adulthood worldwide. The atherosclerotic process starts even before birth, progresses through childhood and, if not stopped, eventually leads to CHD. Therefore, it is important to start prevention from the earliest stages of life. CHD prevention can be performed at different interventional stages: primordial prevention is aimed at preventing risk factors, primary prevention is aimed at early identification and treatment of risk factors, secondary prevention is aimed at reducing the risk of further events in those patients who have already experienced a CHD event. In this context, CHD risk stratification is of utmost importance, in order to tailor the preventive and therapeutic approach. Nutritional intervention is the milestone treatment in pediatric patients at increased CHD risk. According to the Developmental Origin of Health and Disease theory, the origins of lifestyle-related disease is formed in the so called "first thousand days" from conception, when an insult, either positive or negative, can cause life-lasting consequences. Nutrition is a positive epigenetic factor: an adequate nutritional intervention in a developmental critical period can change the outcome from childhood into adulthood.


Assuntos
Doenças Cardiovasculares/prevenção & controle , Transtornos da Nutrição Infantil/dietoterapia , Desnutrição/dietoterapia , Terapia Nutricional , Adolescente , Desenvolvimento do Adolescente , Fatores Etários , Doenças Cardiovasculares/diagnóstico , Doenças Cardiovasculares/fisiopatologia , Criança , Desenvolvimento Infantil , Transtornos da Nutrição Infantil/diagnóstico , Transtornos da Nutrição Infantil/fisiopatologia , Fenômenos Fisiológicos da Nutrição Infantil , Pré-Escolar , Fatores de Risco de Doenças Cardíacas , Humanos , Lactente , Recém-Nascido , Desnutrição/diagnóstico , Desnutrição/fisiopatologia , Estado Nutricional , Prevenção Primária , Medição de Risco , Resultado do Tratamento
8.
Clin Pharmacol Ther ; 110(3): 702-713, 2021 09.
Artigo em Inglês | MEDLINE | ID: mdl-34255863

RESUMO

The African American (AA) population displays a 1.6 to 3-fold higher incidence of thrombosis and stroke mortality compared with European Americans (EAs). Current antiplatelet therapies target the ADP-mediated signaling pathway, which displays significant pharmacogenetic variation for platelet reactivity. The focus of this study was to define underlying population differences in platelet function in an effort to identify novel molecular targets for future antiplatelet therapy. We performed deep coverage RNA-Seq to compare gene expression levels in platelets derived from a cohort of healthy volunteers defined by ancestry determination. We identified > 13,000 expressed platelet genes of which 480 were significantly differentially expressed genes (DEGs) between AAs and EAs. DEGs encoding proteins known or predicted to modulate platelet aggregation, morphology, or platelet count were upregulated in AA platelets. Numerous G-protein coupled receptors, ion channels, and pro-inflammatory cytokines not previously associated with platelet function were likewise differentially expressed. Many of the signaling proteins represent potential pharmacologic targets of intervention. Notably, we confirmed the differential expression of cytokines IL32 and PROK2 in an independent cohort by quantitative real-time polymerase chain reaction, and provide functional validation of the opposing actions of these two cytokines on collagen-induced AA platelet aggregation. Using Genotype-Tissue Expression whole blood data, we identified 516 expression quantitative trait locuses with Fst values > 0.25, suggesting that population-differentiated alleles may contribute to differences in gene expression. This study identifies gene expression differences at the population level that may affect platelet function and serve as potential biomarkers to identify cardiovascular disease risk. Additionally, our analysis uncovers candidate novel druggable targets for future antiplatelet therapies.


Assuntos
Plaquetas/fisiologia , Grupos de Populações Continentais/genética , RNA Mensageiro/genética , Adolescente , Afro-Americanos/genética , Biomarcadores/sangue , Plaquetas/efeitos dos fármacos , Doenças Cardiovasculares/tratamento farmacológico , Doenças Cardiovasculares/genética , Doenças Cardiovasculares/fisiopatologia , Citocinas/genética , Feminino , Expressão Gênica/efeitos dos fármacos , Expressão Gênica/genética , Humanos , Masculino , Inibidores da Agregação Plaquetária/uso terapêutico , Testes de Função Plaquetária/métodos
9.
Am J Physiol Heart Circ Physiol ; 321(2): H435-H445, 2021 08 01.
Artigo em Inglês | MEDLINE | ID: mdl-34242094

RESUMO

Arterial stiffening, a characteristic feature of obesity and type 2 diabetes, contributes to the development and progression of cardiovascular diseases (CVD). Currently, no effective prophylaxis or therapeutics is available to prevent or treat arterial stiffening. A better understanding of the molecular mechanisms underlying arterial stiffening is vital to identify newer targets and strategies to reduce CVD burden. A major contributor to arterial stiffening is increased collagen deposition. In the 5'-untranslated regions of mRNAs encoding for type I collagen, an evolutionally conserved stem-loop (SL) structure plays an essential role in its stability and post-transcriptional regulation. Here, we show that feeding a high-fat/high-sucrose (HFHS) diet for 28 wk increases adiposity, insulin resistance, and blood pressure in male wild-type littermates. Moreover, arterial stiffness, assessed in vivo via aortic pulse wave velocity, and ex vivo using atomic force microscopy in aortic explants or pressure myography in isolated femoral and mesenteric arteries, was also increased in those mice. Notably, all these indices of arterial stiffness, along with collagen type I levels in the vasculature, were reduced in HFHS-fed mice harboring a mutation in the 5'SL structure, relative to wild-type littermates. This protective vascular phenotype in 5'SL-mutant mice did not associate with a reduction in insulin resistance or blood pressure. These findings implicate the 5'SL structure as a putative therapeutic target to prevent or reverse arterial stiffening and CVD associated with obesity and type 2 diabetes.NEW & NOTEWORTHY In the 5'-untranslated (UTR) regions of mRNAs encoding for type I collagen, an evolutionally conserved SL structure plays an essential role in its stability and posttranscriptional regulation. We demonstrate that a mutation of the SL mRNA structure in the 5'-UTR decreases collagen type I deposition and arterial stiffness in obese mice. Targeting this evolutionarily conserved SL structure may hold promise in the management of arterial stiffening and CVD associated with obesity and type 2 diabetes.


Assuntos
Aorta/fisiopatologia , Doenças Cardiovasculares/genética , Colágeno Tipo I/genética , Sequências Repetidas Invertidas/genética , Obesidade/fisiopatologia , RNA Mensageiro/genética , Rigidez Vascular/genética , Regiões 5' não Traduzidas/genética , Adiposidade , Animais , Doenças Cardiovasculares/fisiopatologia , Dieta Hiperlipídica , Sacarose na Dieta , Artéria Femoral/fisiopatologia , Resistência à Insulina , Masculino , Artérias Mesentéricas/fisiopatologia , Camundongos , Microscopia de Força Atômica , Mutação , Análise de Onda de Pulso
10.
Rev Cardiovasc Med ; 22(2): 343-351, 2021 06 30.
Artigo em Inglês | MEDLINE | ID: mdl-34258902

RESUMO

Coronavirus disease 2019 (COVID-19), a mystified cryptic virus has challenged the mankind that has brought life to a standstill. Catastrophic loss of life, perplexed healthcare system and the downfall of global economy are some of the outcomes of this pandemic. Humans are raging a war with an unknown enemy. Infections, irrespective of age and gender, and more so in comorbidities are escalating at an alarming rate. Cardiovascular diseases, are the leading cause of death globally with an estimate of 31% of deaths worldwide out of which nearly 85% are due to heart attacks and stroke. Theoretically and practically, researchers have observed that persons with pre-existing cardiovascular conditions are comparatively more vulnerable to the COVID-19 infection. Moreover, they have studied the data between less severe and more severe cases, survivors and non survivors, intensive care unit (ICU) patients and non ICU patients, to analyse the relationship and the influence of COVID-19 on cardiovascular health of an individual, further the risk of susceptibility to submit to the virus. This review aims to provide a comprehensive particular on the possible effects, either direct or indirect, of COVID-19 on the cardiovascular heath of an individual.


Assuntos
COVID-19/virologia , Doenças Cardiovasculares/virologia , Sistema Cardiovascular/virologia , SARS-CoV-2/patogenicidade , Antivirais/uso terapêutico , COVID-19/tratamento farmacológico , COVID-19/mortalidade , COVID-19/fisiopatologia , COVID-19/terapia , Fármacos Cardiovasculares/uso terapêutico , Doenças Cardiovasculares/mortalidade , Doenças Cardiovasculares/fisiopatologia , Doenças Cardiovasculares/terapia , Sistema Cardiovascular/efeitos dos fármacos , Sistema Cardiovascular/fisiopatologia , Comorbidade , Interações Hospedeiro-Patógeno , Humanos , Prognóstico , Medição de Risco , Fatores de Risco , SARS-CoV-2/efeitos dos fármacos
11.
Arterioscler Thromb Vasc Biol ; 41(9): 2357-2369, 2021 09.
Artigo em Inglês | MEDLINE | ID: mdl-34196216

RESUMO

Endothelial-to-mesenchymal transition is a dynamic process in which endothelial cells suppress constituent endothelial properties and take on mesenchymal cell behaviors. To begin the process, endothelial cells loosen their cell-cell junctions, degrade the basement membrane, and migrate out into the perivascular surroundings. These initial endothelial behaviors reflect a transient modulation of cellular phenotype, that is, a phenotypic modulation, that is sometimes referred to as partial endothelial-to-mesenchymal transition. Loosening of endothelial junctions and migration are also seen in inflammatory and angiogenic settings such that endothelial cells initiating endothelial-to-mesenchymal transition have overlapping behaviors and gene expression with endothelial cells responding to inflammatory signals or sprouting to form new blood vessels. Reduced endothelial junctions increase permeability, which facilitates leukocyte trafficking, whereas endothelial migration precedes angiogenic sprouting and neovascularization; both endothelial barriers and quiescence are restored as inflammatory and angiogenic stimuli subside. Complete endothelial-to-mesenchymal transition proceeds beyond phenotypic modulation such that mesenchymal characteristics become prominent and endothelial functions diminish. In proadaptive, regenerative settings the new mesenchymal cells produce extracellular matrix and contribute to tissue integrity whereas in maladaptive, pathologic settings the new mesenchymal cells become fibrotic, overproducing matrix to cause tissue stiffness, which eventually impacts function. Here we will review what is known about how TGF (transforming growth factor) ß influences this continuum from junctional loosening to cellular migration and its relevance to cardiovascular diseases.


Assuntos
Doenças Cardiovasculares/patologia , Células Endoteliais/patologia , Endotélio Vascular/patologia , Transição Epitelial-Mesenquimal , Animais , Doenças Cardiovasculares/metabolismo , Doenças Cardiovasculares/fisiopatologia , Movimento Celular , Células Endoteliais/metabolismo , Endotélio Vascular/metabolismo , Endotélio Vascular/fisiopatologia , Humanos , Permeabilidade , Fenótipo , Transdução de Sinais
12.
Am J Cardiol ; 152: 146-149, 2021 08 01.
Artigo em Inglês | MEDLINE | ID: mdl-34237610

RESUMO

The optimal screening strategy to prevent sudden cardiac death (SCD) in athletes remains unknown. Pre-participation screening with electrocardiogram (ECG) remains controversial. The utility and accuracy of limb-lead (LL) ECG alone in identifying cardiac abnormalities associated with SCD has not been studied. This study was a comparative secondary data analysis, comparing the interpretation accuracy of 4 physicians evaluating publicly available ECGs of the most common cardiac conditions associated with SCD in athletes. Each physician interpreted a total of 100 ECGs: 50 normal ECGs (25 LL and 25 standard 12L) and 50 abnormal ECGs (25 LL and 25 standard 12L). The agreement between LL ECGs and 12L ECGs was assessed by Cohen's kappa coefficient and the accuracy of identifying an abnormal ECG was compared across LL and 12L ECGs using a chi-squared test. Inter-rater reliability was assessed by estimating the Fleiss's kappa coefficient. The sensitivity of LL ECG and 12L ECG was identical at 86%. The specificity of LL ECG was 75% (95% CI = 65% to 83%) and 12L ECG was 82% (95% CI = 73% to 89%). Substantial agreement was seen between LL ECG and 12L ECG interpretation across all readers (k = 0.63; 95% CI = 0.49 to 0.77). Interpretation accuracy was 81% (95% CI = 74% to 86%) and 84% (95% CI 78% to 89%) using LL ECG and 12L ECG, respectively (p = 0.43). In conclusion, the accuracy, sensitivity, and specificity were high and comparable for both LL ECG and 12L ECG in identifying cardiovascular conditions associated with SCD. Agreement between LL ECG and 12L ECG was substantial.


Assuntos
Atletas , Doenças Cardiovasculares/diagnóstico , Morte Súbita Cardíaca/prevenção & controle , Eletrocardiografia/métodos , Displasia Arritmogênica Ventricular Direita/complicações , Displasia Arritmogênica Ventricular Direita/diagnóstico , Displasia Arritmogênica Ventricular Direita/fisiopatologia , Síndrome de Brugada/complicações , Síndrome de Brugada/diagnóstico , Síndrome de Brugada/fisiopatologia , Cardiomiopatia Dilatada/complicações , Cardiomiopatia Dilatada/diagnóstico , Cardiomiopatia Dilatada/fisiopatologia , Cardiomiopatia Hipertrófica/complicações , Cardiomiopatia Hipertrófica/diagnóstico , Cardiomiopatia Hipertrófica/fisiopatologia , Doenças Cardiovasculares/complicações , Doenças Cardiovasculares/fisiopatologia , Morte Súbita Cardíaca/etiologia , Humanos , Síndrome do QT Longo/complicações , Síndrome do QT Longo/diagnóstico , Síndrome do QT Longo/fisiopatologia , Programas de Rastreamento , Miocardite/complicações , Miocardite/diagnóstico , Miocardite/fisiopatologia , Síndrome de Wolff-Parkinson-White/complicações , Síndrome de Wolff-Parkinson-White/diagnóstico , Síndrome de Wolff-Parkinson-White/fisiopatologia
13.
Life Sci ; 283: 119841, 2021 Oct 15.
Artigo em Inglês | MEDLINE | ID: mdl-34298036

RESUMO

Sympathetic vasomotor overactivity is a major feature leading to the cardiovascular dysfunction related to obesity. Considering that the retroperitoneal white adipose tissue (rWAT) is an important fat visceral depot and receives intense sympathetic and afferent innervations, the present study aimed to evaluate the effects evoked by bilateral rWAT denervation in obese rats. Male Wistar rats were fed with HFD for 8 consecutive weeks and rWAT denervation was performed at the 6th week. Arterial pressure, splanchnic and renal sympathetic vasomotor nerve activities were assessed and inflammation and the components of the renin -angiotensin system were evaluated in different white adipose tissue depots. HFD animals presented higher serum levels of leptin and glucose, an increase in arterial pressure and splanchnic sympathetic nerve activity; rWAT denervation, normalized these parameters. Pro-inflammatory cytokines levels were significantly increased, as well as RAAS gene expression in WAT of HFD animals; rWAT denervation significantly attenuated these changes. In conclusion, HFD promotes vasomotor sympathetic overactivation and inflammation with repercussions on the cardiovascular system. In conclusion, the neural communication between WAT and the brain is fundamental to trigger sympathetic vasomotor activation and this pathway is a possible new therapeutic target to treat obesity-associated cardiovascular dysfunction.


Assuntos
Doenças Cardiovasculares , Denervação , Dieta Hiperlipídica/efeitos adversos , Gordura Intra-Abdominal , Obesidade , Nervos Esplâncnicos , Animais , Pressão Sanguínea , Doenças Cardiovasculares/metabolismo , Doenças Cardiovasculares/fisiopatologia , Doenças Cardiovasculares/terapia , Sistema Cardiovascular/metabolismo , Sistema Cardiovascular/fisiopatologia , Gordura Intra-Abdominal/inervação , Gordura Intra-Abdominal/metabolismo , Gordura Intra-Abdominal/fisiopatologia , Masculino , Obesidade/induzido quimicamente , Obesidade/metabolismo , Obesidade/fisiopatologia , Obesidade/terapia , Ratos , Ratos Wistar , Sistema Renina-Angiotensina , Nervos Esplâncnicos/metabolismo , Nervos Esplâncnicos/patologia , Nervos Esplâncnicos/fisiopatologia
14.
Biomolecules ; 11(6)2021 06 11.
Artigo em Inglês | MEDLINE | ID: mdl-34207942

RESUMO

Blood pressure (BP) follows a circadian rhythm, it increases on waking in the morning and decreases during sleeping at night. Disruption of the circadian BP rhythm has been reported to be associated with worsened cardiovascular and renal outcomes, however the underlying molecular mechanisms are still not clear. In this review, we briefly summarized the current understanding of the circadian BP regulation and provided therapeutic overview of the relationship between circadian BP rhythm and cardiovascular and renal health and disease.


Assuntos
Pressão Sanguínea/fisiologia , Doenças Cardiovasculares/fisiopatologia , Ritmo Circadiano/fisiologia , Nefropatias/fisiopatologia , Doenças Cardiovasculares/metabolismo , Sistema Cardiovascular/fisiopatologia , China , Humanos , Hipertensão/fisiopatologia , Rim/fisiopatologia , Nefropatias/metabolismo
15.
Eur J Endocrinol ; 185(4): 507-514, 2021 Aug 27.
Artigo em Inglês | MEDLINE | ID: mdl-34324433

RESUMO

Background: Despite adequate presurgical management, blood pressure fluctuations are common during resection of pheochromocytoma or sympathetic paraganglioma (PPGL). To a large extent, the variability in blood pressure control during PPGL resection remains unexplained. Adrenomedullin and B-type natriuretic peptide, measured as MR-proADM and NT-proBNP, respectively, are circulating biomarkers of cardiovascular dysfunction. We investigated whether plasma levels of MR-proADM and NT-proBNP are associated with blood pressure fluctuations during PPGL resection. Methods: Study subjects participated in PRESCRIPT, a randomized controlled trial in patients undergoing PPGL resection. MR-proADM and NT-proBNP were determined in a single plasma sample drawn before surgery. Multivariable linear and logistic regression analyses were used to explore associations between these biomarkers and blood pressure fluctuations, use of vasoconstrictive agents during surgery as well as the occurrence of perioperative cardiovascular events. Results: A total of 126 PPGL patients were included. Median plasma concentrations of MR-proADM and NT-proBNP were 0.51 (0.41-0.63) nmol/L and 68.7 (27.9-150.4) ng/L, respectively. Neither MR-proADM nor NT-proBNP were associated with blood pressure fluctuations. There was a positive correlation between MR-proADM concentration and the cumulative dose of vasoconstrictive agents (03B2 0.44, P =0.001). Both MR-proADM and NT-proBNP were significantly associated with perioperative cardiovascular events (OR: 5.46, P =0.013 and OR: 1.54, P =0.017, respectively). Conclusions: plasma MR-proADM or NT-proBNP should not be considered as biomarkers for the presurgical risk assessment of blood pressure fluctuations during PPGL resection. Future studies are needed to explore the potential influence of these biomarkers on the intraoperative requirement of vasoconstrictive agents and the perioperative cardiovascular risk.


Assuntos
Neoplasias das Glândulas Suprarrenais , Adrenomedulina/sangue , Pressão Sanguínea/fisiologia , Peptídeo Natriurético Encefálico/sangue , Feocromocitoma , Neoplasias das Glândulas Suprarrenais/sangue , Neoplasias das Glândulas Suprarrenais/diagnóstico , Neoplasias das Glândulas Suprarrenais/tratamento farmacológico , Neoplasias das Glândulas Suprarrenais/cirurgia , Antagonistas Adrenérgicos/uso terapêutico , Adulto , Idoso , Biomarcadores/sangue , Doenças Cardiovasculares/sangue , Doenças Cardiovasculares/diagnóstico , Doenças Cardiovasculares/fisiopatologia , Doenças Cardiovasculares/prevenção & controle , Estudos Transversais , Feminino , Seguimentos , Insuficiência Cardíaca/sangue , Insuficiência Cardíaca/diagnóstico , Insuficiência Cardíaca/fisiopatologia , Insuficiência Cardíaca/prevenção & controle , Humanos , Complicações Intraoperatórias/sangue , Complicações Intraoperatórias/diagnóstico , Complicações Intraoperatórias/fisiopatologia , Complicações Intraoperatórias/prevenção & controle , Masculino , Pessoa de Meia-Idade , Feocromocitoma/sangue , Feocromocitoma/diagnóstico , Feocromocitoma/tratamento farmacológico , Feocromocitoma/cirurgia , Prognóstico , Medição de Risco , Resultado do Tratamento
16.
Int J Mol Sci ; 22(14)2021 Jul 14.
Artigo em Inglês | MEDLINE | ID: mdl-34299174

RESUMO

Fetal growth restriction (FGR) is a common complication of pregnancy, resulting in a fetus that fails to reach its genetically determined growth potential. Whilst the fetal cardiovascular response to acute hypoxia is well established, the fetal defence to chronic hypoxia is not well understood due to experiment constraints. Growth restriction results primarily from reduced oxygen and nutrient supply to the developing fetus, resulting in chronic hypoxia. The fetus adapts to chronic hypoxia by redistributing cardiac output via brain sparing in an attempt to preserve function in the developing brain. This review highlights the impact of brain sparing on the developing fetal cardiovascular and cerebrovascular systems, as well as emerging long-term effects in offspring that were growth restricted at birth. Here, we explore the pathogenesis associated with brain sparing within the cerebrovascular system. An increased understanding of the mechanistic pathways will be critical to preventing neuropathological outcomes, including motor dysfunction such as cerebral palsy, or behaviour dysfunctions including autism and attention-deficit/hyperactivity disorder (ADHD).


Assuntos
Doenças Cardiovasculares/fisiopatologia , Transtornos Cerebrovasculares/fisiopatologia , Retardo do Crescimento Fetal/patologia , Hipóxia/fisiopatologia , Débito Cardíaco , Feminino , Retardo do Crescimento Fetal/etiologia , Retardo do Crescimento Fetal/terapia , Humanos , Recém-Nascido , Gravidez
17.
Int J Mol Sci ; 22(12)2021 Jun 20.
Artigo em Inglês | MEDLINE | ID: mdl-34203038

RESUMO

Heavy metals are toxic environmental pollutants associated with severe ecological and human health risks. Among them is mercury (Hg), widespread in air, soil, and water, due to its peculiar geo-biochemical cycle. The clinical consequences of Hg exposure include neurotoxicity and nephrotoxicity. Furthermore, increased risk for cardiovascular diseases is also reported due to a direct effect on cardiovascular tissues, including endothelial cells, recently identified as important targets for the harmful action of heavy metals. In this review, we will discuss the rationale for the potential use of erythrocytes as a surrogate model to study Hg-related toxicity on the cardiovascular system. The toxic effects of Hg on erythrocytes have been amply investigated in the last few years. Among the observed alterations, phosphatidylserine exposure has been proposed as an underlying mechanism responsible for Hg-induced increased proatherogenic and prothrombotic activity of these cells. Furthermore, following Hg-exposure, a decrease in NOS activity has also been reported, with consequent lowering of NO bioavailability, thus impairing endothelial function. An additional mechanism that may induce a decrease in NO availability is the generation of an oxidative microenvironment. Finally, considering that chronic Hg exposure mainly occurs through contaminated foods, the protective effect of dietary components is also discussed.


Assuntos
Vasos Sanguíneos/efeitos dos fármacos , Vasos Sanguíneos/fisiopatologia , Eritrócitos/efeitos dos fármacos , Eritrócitos/metabolismo , Metais Pesados/toxicidade , Animais , Vasos Sanguíneos/metabolismo , Doenças Cardiovasculares/etiologia , Doenças Cardiovasculares/metabolismo , Doenças Cardiovasculares/fisiopatologia , Sistema Cardiovascular/efeitos dos fármacos , Sistema Cardiovascular/metabolismo , Sistema Cardiovascular/fisiopatologia , Suscetibilidade a Doenças , Endotélio/efeitos dos fármacos , Endotélio/metabolismo , Poluentes Ambientais/efeitos adversos , Humanos , Mercúrio/toxicidade , Oxirredução/efeitos dos fármacos , Estresse Oxidativo/efeitos dos fármacos
18.
Int J Mol Sci ; 22(13)2021 Jun 23.
Artigo em Inglês | MEDLINE | ID: mdl-34201646

RESUMO

The physiological and pathophysiological relevance of the angiotensin II type 1 (AT1) G protein-coupled receptor no longer needs to be proven in the cardiovascular system. The renin-angiotensin system and the AT1 receptor are the targets of several classes of therapeutics (such as angiotensin converting enzyme inhibitors or angiotensin receptor blockers, ARBs) used as first-line treatments in cardiovascular diseases. The importance of AT1 in the regulation of the cerebrovascular system is also acknowledged. However, despite numerous beneficial effects in preclinical experiments, ARBs do not induce satisfactory curative results in clinical stroke studies. A better understanding of AT1 signaling and the development of biased AT1 agonists, able to selectively activate the ß-arrestin transduction pathway rather than the Gq pathway, have led to new therapeutic strategies to target detrimental effects of AT1 activation. In this paper, we review the involvement of AT1 in cerebrovascular diseases as well as recent advances in the understanding of its molecular dynamics and biased or non-biased signaling. We also describe why these alternative signaling pathways induced by ß-arrestin biased AT1 agonists could be considered as new therapeutic avenues for cerebrovascular diseases.


Assuntos
Bloqueadores do Receptor Tipo 1 de Angiotensina II/farmacologia , Doenças Cardiovasculares/tratamento farmacológico , Receptor Tipo 1 de Angiotensina/química , Receptor Tipo 1 de Angiotensina/metabolismo , Animais , Lesões Encefálicas Traumáticas/metabolismo , Doenças Cardiovasculares/metabolismo , Doenças Cardiovasculares/fisiopatologia , Humanos , Aneurisma Intracraniano/metabolismo , Terapia de Alvo Molecular/métodos , Transdução de Sinais/efeitos dos fármacos , Acidente Vascular Cerebral/metabolismo , beta-Arrestinas/agonistas , beta-Arrestinas/metabolismo
19.
Int J Mol Sci ; 22(14)2021 Jul 16.
Artigo em Inglês | MEDLINE | ID: mdl-34299240

RESUMO

Glucocorticoids are steroid hormones with key roles in the regulation of many physiological systems including energy homeostasis and immunity. However, chronic glucocorticoid excess, highlighted in Cushing's syndrome, is established as being associated with increased cardiovascular disease (CVD) risk. Atherosclerosis is the major cause of CVD, leading to complications including coronary artery disease, myocardial infarction and heart failure. While the associations between glucocorticoid excess and increased prevalence of these complications are well established, the mechanisms underlying the role of glucocorticoids in development of atheroma are unclear. This review aims to better understand the importance of glucocorticoids in atherosclerosis and to dissect their cell-specific effects on key processes (e.g., contractility, remodelling and lesion development). Clinical and pre-clinical studies have shown both athero-protective and pro-atherogenic responses to glucocorticoids, effects dependent upon their multifactorial actions. Evidence indicates regulation of glucocorticoid bioavailability at the vasculature is complex, with local delivery, pre-receptor metabolism, and receptor expression contributing to responses linked to vascular remodelling and inflammation. Further investigations are required to clarify the mechanisms through which endogenous, local glucocorticoid action and systemic glucocorticoid treatment promote/inhibit atherosclerosis. This will provide greater insights into the potential benefit of glucocorticoid targeted approaches in the treatment of cardiovascular disease.


Assuntos
Aterosclerose/tratamento farmacológico , Aterosclerose/fisiopatologia , Glucocorticoides/farmacologia , Aterosclerose/metabolismo , Doenças Cardiovasculares/tratamento farmacológico , Doenças Cardiovasculares/etiologia , Doenças Cardiovasculares/fisiopatologia , Síndrome de Cushing , Glucocorticoides/metabolismo , Humanos , Inflamação/tratamento farmacológico , Receptores de Glucocorticoides/metabolismo , Fatores de Risco
20.
Ecotoxicol Environ Saf ; 220: 112397, 2021 Sep 01.
Artigo em Inglês | MEDLINE | ID: mdl-34116334

RESUMO

BACKGROUND: Decline in pulmonary function contributes to increasing cardiovascular disease (CVD) risk. Although adverse effects of short-term exposure to fine particulate matter (PM2.5) on pulmonary function have been recognized in healthy people or patients with respiratory disease, these results were not well illustrated among people with elevated CVD risk. MATERIALS AND METHODS: A panel study was conducted in three Chinese cities with three repeated visits among populations at intermediate to high-risk of CVD, defined as treated hypertension patients or those with blood pressure ≥ 130/80 mmHg, who met any of the three conditions including abdominal obesity, dyslipidemia, and diabetes mellitus. Individualized PM2.5 exposure and pulmonary function were measured during each seasonal visit. Linear mixed-effect models were applied to analyze the associations of PM2.5 concentrations with pulmonary function indicators, including forced expiratory volume in 1 s (FEV1), FEV1/forced vital capacity (FVC), maximal mid-expiratory flow (MMF), and peak expiratory flow (PEF). RESULTS: Short-term PM2.5 exposure was significantly associated with decreased pulmonary function and an increment of 10 µg/m3 in PM2.5 concentrations during lag 12-24 hour was associated with declines of 41.7 ml/s (95% confidence interval [CI]: 7.7-75.7), 0.35% (95% CI: 0.01, 0.69), and 20.9 ml/s (95% CI: 0.5-41.3) for PEF, FEV1/FVC, and MMF, respectively. Results from stratified and sensitivity analyses were generally similar with the overall findings, while the adverse effects of PM2.5 on pulmonary functions were more pronounced in those who were physically inactive. CONCLUSIONS: This study first identified short-term exposure to PM2.5 was associated with impaired pulmonary function and physical activity might attenuate the adverse effects of PM2.5 among populations at intermediate to high-risk of CVD. These findings provide new robust evidence on health effects of air pollution and call for effective prevention measures among people at CVD risk.


Assuntos
Poluentes Atmosféricos/efeitos adversos , Poluição do Ar/efeitos adversos , Doenças Cardiovasculares/fisiopatologia , Exposição Ambiental/efeitos adversos , Pulmão/efeitos dos fármacos , Material Particulado/efeitos adversos , Testes de Função Respiratória , Adulto , Poluentes Atmosféricos/análise , Poluição do Ar/análise , Pressão Sanguínea , Doenças Cardiovasculares/induzido quimicamente , China , Cidades , Exposição Ambiental/análise , Volume Expiratório Forçado , Humanos , Masculino , Pessoa de Meia-Idade , Material Particulado/análise , Fatores de Risco , Capacidade Vital
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