Search results for "endothelial dysfunction"

showing 10 items of 287 documents

Critical role of fractalkine (CX3CL1) in cigarette smoke-induced mononuclear cell adhesion to the arterial endothelium.

2012

Background Cigarette smoking is an important risk factor for the development of cardiovascular disease, yet the pathways through which this may operate are poorly understood. Therefore, the mechanism underlying cigarette smoke (CS)-induced arterial endothelial dysfunction and the potential link with fractalkine/CX3CL1 upregulation were investigated. Methods and results Stimulation of human arterial umbilical endothelial cells (HUAECs) with pathophysiological concentrations of CS extract (1% CSE) increased CX3CL1 expression. Neutralisation of CX3CL1 activity under dynamic flow conditions significantly inhibited CSE-induced mononuclear cell adhesion to HUAECs (67%). The use of small interferi…

Pulmonary and Respiratory Medicinemedicine.medical_specialtyEndotheliumPeripheral blood mononuclear cellMiceInternal medicineCX3CR1Cell AdhesionMedicineAnimalsHumansEndothelial dysfunctionRNA Small InterferingCell adhesionNADPH oxidasebiologybusiness.industryChemokine CX3CL1MicrocirculationSmokingNOX4Membrane ProteinsNADPH Oxidasesmedicine.diseaseUp-RegulationEndothelial stem cellmedicine.anatomical_structureEndocrinologyNADPH Oxidase 5Immunologybiology.proteinEndothelium VascularbusinessThorax
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Could E-cigarette vaping contribute to heart disease?

2020

E-cigarettes have become a controversial topic. While their benefits are questioned by the scientific community, a part of the medical profession is still supporting them as an effective harm reduction tool for smoking cessation. The impact of E-cigarettes on the cardiovascular system is still elusive.We assessed results from animal, pre(clinical), and epidemiological studies to critically evaluate and synthesize evidence relevant to the cardiovascular effects of E-cigarettes. Animal studies have demonstrated that E-cigarette vapor exposure can cause endothelial and cardiac dysfunction. However, there have also been reports on the less harmful effects of E-cigarette vapor exposure in compar…

Pulmonary and Respiratory Medicinemedicine.medical_specialtyHeart diseaseHeart DiseasesElectronic Nicotine Delivery Systemsmedicine.disease_cause03 medical and health sciences0302 clinical medicinemedicineTobacco SmokingImmunology and AllergyAnimalsHumans030212 general & internal medicineEndothelial dysfunctionIntensive care medicineInhalation Exposurebusiness.industryVapingPublic Health Environmental and Occupational Healthmedicine.diseaseHarm030228 respiratory systemMedical professionSmoking CessationbusinessOxidative stressExpert review of respiratory medicine
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Arterial stiffness in symptomatic smokers with normal lung function

2017

Chronic obstructive pulmonary disease (COPD) is associated with cardiovascular morbidity and mortality. Arterial stiffness and endothelial dysfunction index are validated surrogate cardiovascular markers and are increased in subjects with COPD. We tested whether increased arterial stiffness and endothelial dysfunction occur in symptomatic smokers with no evidence of bronchial obstruction. Clinical and lung functional assessments were conducted in smoker subjects with chronic respiratory symptoms and in COPD patients. Pulse wave velocity (PWV), aortic augmentation index (AIx) and reactive hyperaemia index (RHI) were measured to estimate the cardiovascular risk. 48 smokers (male n=37, female …

Pulmonary and Respiratory Medicinemedicine.medical_specialtyPathology1lcsh:Medicine030204 cardiovascular system & hematologySettore MED/10 - Malattie Dell'Apparato Respiratorio03 medical and health sciencesHyperaemia0302 clinical medicineInternal medicinemedicineEndothelial dysfunctionRespiratory systemPulse wave velocityCOPDLungbusiness.industrylcsh:ROriginal ArticlesAortic Augmentation Indexmedicine.diseaserespiratory tract diseasesmedicine.anatomical_structure030228 respiratory systemCardiologyArterial stiffnessmedicine.symptombusiness
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Novel therapeutical approaches to managing atherosclerotic risk

2021

Atherosclerosis is a multifactorial vascular disease that leads to inflammation and stiffening of the arteries and decreases their elasticity due to the accumulation of calcium, small dense Low Density Lipoproteins (sdLDL), inflammatory cells, and fibrotic material. A review of studies pertaining to cardiometabolic risk factors, lipids alterations, hypolipidemic agents, nutraceuticals, hypoglycaemic drugs, atherosclerosis, endothelial dysfunction, and inflammation was performed. There are several therapeutic strategies including Proprotein Convertase Subtilisin/Kexin 9 (PCSK9) inhibitors, inclisiran, bempedoic acid, Glucagon-Like Peptide-1 Receptor agonists (GLP-1 RAs), and nutraceuticals t…

QH301-705.5InflammationReview030204 cardiovascular system & hematologyPharmacologyCatalysisInorganic Chemistry03 medical and health sciences0302 clinical medicineLipid oxidationmedicineAnimalsHumans030212 general & internal medicineMolecular Targeted TherapyPhysical and Theoretical ChemistryEndothelial dysfunctionBiology (General)Molecular BiologyQD1-999SpectroscopyInnovative therapiesMolecular signalingVascular diseasebusiness.industryPCSK9Organic ChemistryGeneral MedicineProprotein convertasemedicine.diseaseAtherosclerosisComputer Science ApplicationsManagementChemistryInflammationsAtheromaOxidative stressHypolipidemic Agentslipids (amino acids peptides and proteins)Nutraceuticalsmedicine.symptombusiness
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Inhibition of Rac1 GTPase Decreases Vascular Oxidative Stress, Improves Endothelial Function, and Attenuates Atherosclerosis Development in Mice

2021

Aims: Oxidative stress and inflammation contribute to atherogenesis. Rac1 GTPase regulates pro-oxidant NADPH oxidase activity, reactive oxygen species (ROS) formation, actin cytoskeleton organization and monocyte adhesion. We investigated the vascular effects of pharmacological inhibition of Rac1 GTPase in mice.Methods and Results: We treated wild-type and apolipoprotein E-deficient (ApoE−/−) mice with Clostridium sordellii lethal toxin (LT), a Rac1 inhibitor, and assessed vascular oxidative stress, expression and activity of involved proteins, endothelial function, macrophage infiltration, and atherosclerosis development. LT-treated wild-type mice displayed decreased vascular NADPH oxidase…

RHOAInflammationVascular permeabilityfree radicalsPharmacologyCardiovascular Medicinemedicine.disease_causeActin cytoskeleton organizationendothelial functionmedicineoxidative stressDiseases of the circulatory (Cardiovascular) systemddc:610Endothelial dysfunctionOriginal Researchchemistry.chemical_classificationReactive oxygen speciesNADPH oxidaseGTPasesbiologymedicine.diseasechemistryatherosclerosis endothelial function oxidative stress free radicals Rac1 GTPasesRC666-701biology.proteinmedicine.symptomatherosclerosisCardiology and Cardiovascular MedicineOxidative stressRac1Frontiers in Cardiovascular Medicine
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Peripheral artery disease: potential role of ACE-inhibitor therapy

2008

Giuseppe Coppola, Giuseppe Romano, Egle Corrado, Rosa Maria Grisanti, Salvatore NovoDepartment of Internal Medicine, Cardiovascular and Nephro-Urological Diseases, Chair of Cardiovascular Disease, University of Palermo, Palermo, ItalyAbstract: Subjects with peripheral arterial disease (PAD) of the lower limbs are at high risk for cardiovascular and cerebrovascular events and the prevalence of coronary artery disease in such patients is elevated. Recent studies have shown that regular use of cardiovascular medications, such as therapeutic and preventive agents for PAD patients, seems to be promising in reducing long-term mortality and morbidity. The angiotensin-converting-enzyme (ACE) system…

Ramiprillcsh:Diseases of the circulatory (Cardiovascular) systemmedicine.medical_specialtyPathologyACE inhibitorsEndocrinology Diabetes and MetabolismBradykininAngiotensin-Converting Enzyme InhibitorsReviewDiseaseendothelial dysfunctionCoronary artery diseasechemistry.chemical_compoundperipheral arterial diseaseInternal medicineHumansMedicinePharmacology (medical)Endothelial dysfunctionCell ProliferationSubclinical infectionPeripheral Vascular Diseasesbusiness.industryFibrinolysisPublic Health Environmental and Occupational HealthCardiovascular AgentsPeripheral artery disease ACE-inhibitorintermittent claudicationHematologyGeneral Medicinemedicine.diseaseSettore MED/11 - Malattie Dell'Apparato Cardiovascolareperipheral arterial disease.Oxidative StressTreatment OutcomeLower ExtremitychemistryCardiovascular Diseaseslcsh:RC666-701ACE-inhibitorsACE inhibitorCardiovascular agentCardiologyEndothelium VascularatherosclerosisCardiology and Cardiovascular Medicinebusinessmedicine.drugVascular Health and Risk Management
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Short-Time Ocular Ischemia Induces Vascular Endothelial Dysfunction and Ganglion Cell Loss in the Pig Retina

2019

Visual impairment and blindness are often caused by retinal ischemia-reperfusion (I/R) injury. We aimed to characterize a new model of I/R in pigs, in which the intraocular pathways were not manipulated by invasive methods on the ocular system. After 12 min of ischemia followed by 20 h of reperfusion, reactivity of retinal arterioles was measured in vitro by video microscopy. Dihydroethidium (DHE) staining, qPCR, immunohistochemistry, quantification of neurons in the retinal ganglion cell layer, and histological examination was performed. Retinal arterioles of I/R-treated pigs displayed marked attenuation in response to the endothelium-dependent vasodilator, bradykinin, compared to sham-tre…

Retinal Ganglion CellsVascular Endothelial Growth Factor A0301 basic medicinePathologySwineNitric Oxide Synthase Type IIVasodilationendothelial dysfunctionlcsh:Chemistrychemistry.chemical_compound0302 clinical medicineIschemiaEndothelial dysfunctionlcsh:QH301-705.5SpectroscopyGeneral MedicineComputer Science ApplicationsArteriolesmedicine.anatomical_structureRetinal ganglion cellReperfusion InjuryNADPH Oxidase 2medicine.medical_specialtyEndotheliumRetinal ArteryI/R injuryIschemiaretinal arteriolesBradykininRetinal ganglionRetinaArticleCatalysisganglion cell lossInorganic Chemistry03 medical and health sciencesmedicineAnimalsPhysical and Theoretical ChemistryMolecular BiologyRetinabusiness.industryOrganic ChemistryRetinalHypoxia-Inducible Factor 1 alpha Subunitmedicine.disease030104 developmental biologylcsh:Biology (General)lcsh:QD1-999chemistry030221 ophthalmology & optometryEndothelium VascularReactive Oxygen SpeciesbusinessInternational Journal of Molecular Sciences
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Pathogenesis and molecular mechanisms of anderson–fabry disease and possible new molecular addressed therapeutic strategies

2021

Anderson–Fabry disease (AFD) is a rare disease with an incidenceof approximately 1:117,000 male births. Lysosomal accumulation of globotriaosylceramide (Gb3) is the element characterizing Fabry disease due to a hereditary deficiency α-galactosidase A (GLA) enzyme. The accumulation of Gb3 causes lysosomal dysfunction that compromises cell signaling pathways. Deposition of sphingolipids occurs in the autonomic nervous system, dorsal root ganglia, kidney epithelial cells, vascular system cells, and myocardial cells, resulting in organ failure. This manuscript will review the molecular pathogenetic pathways involved in Anderson–Fabry disease and in its organ damage. Some studies reported that i…

ReviewConstriction Pathologicendothelial dysfunctionPathogenesisMicechemistry.chemical_compoundKCa3.1 activitypodocyturiaProtein IsoformsEndothelial dysfunctionBiology (General)SpectroscopyglobotriaosylceramideGlobosidesMicrogliabiologyTOR Serine-Threonine KinasesTrihexosylceramidesmiR-26a-5pGeneral MedicineMitochondriaComputer Science ApplicationsCell biologymiR-152-5pChemistrymedicine.anatomical_structureCerebrovascular CirculationAnderson–Fabry disease Endothelial dysfunction Globotriaosylceramide KCa3.1 activity MiR-1307-5p MiR-152-5p MiR-21-5p MiR-26a-5p Podocyturia Valvular dysfunctionmiR-21-5pSignal TransductionQH301-705.5GlobotriaosylceramideCatalysisInorganic ChemistryAutophagymedicineAnimalsHumansEnzyme Replacement TherapyPhysical and Theoretical ChemistryMolecular BiologyMechanistic target of rapamycinQD1-999PI3K/AKT/mTOR pathwaySphingolipidsAnderson–Fabry diseasebusiness.industryMicrocirculationOrganic ChemistryEndothelial Cellsmedicine.diseaseFabry diseaseSphingolipidMicroRNAschemistrymiR-1307-5palpha-Galactosidasebiology.proteinFabry DiseaseGlycolipidsvalvular dysfunctionLysosomesbusiness
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Oxidative stress in cardiovascular disease: successful translation from bench to bedside?

2007

Over the last decades, sound evidence has been generated that oxidative stress is one of the most potent inductors of endothelial dysfunction and is involved at all stages of atherosclerotic plaque evolution.1,2 Experimental and animal models provide a clear association between the amount of oxidative challenge and reversible vascular dysfunction that can be observed before permanent alterations of the vessel wall occur. Article p 1367 Important for cardiovascular biology is the consumption of nitric oxide (NO) by reactive oxygen species. Endothelium relaxant factor is a central molecule in vascular homeostasis as a modulator of endothelial tone and reactivity.3 It is produced by NO synthas…

RiskEndotheliumOxidative phosphorylation030204 cardiovascular system & hematologyPharmacologymedicine.disease_causeArginineNitric OxideNitric oxide03 medical and health scienceschemistry.chemical_compound0302 clinical medicinePhysiology (medical)medicineHumansEndothelial dysfunction030304 developmental biologychemistry.chemical_classification0303 health sciencesReactive oxygen speciesbiologybusiness.industryThrombosismedicine.diseaseAtherosclerosis3. Good healthVasodilationOxidative Stressmedicine.anatomical_structurechemistryCardiovascular DiseasesMyeloperoxidaseImmunologyHemorheologybiology.proteinEndothelium VascularCardiology and Cardiovascular MedicinebusinessReactive Oxygen SpeciesPeroxynitriteOxidative stressBiomarkersCirculation
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Vascular aging in rodent models: contrasting mechanisms driving the female and male vascular senescence

2021

Increasing scientific interest has been directed to sex as a biological and decisive factor on several diseases. Several different mechanisms orchestrate vascular function, as well as vascular dysfunction in cardiovascular and metabolic diseases in males and females. Certain vascular sex differences are present throughout life, while others are more evident before the menopause, suggesting two important and correlated drivers: genetic and hormonal factors. With the increasing life expectancy and aging population, studies on aging-related diseases and aging-related physiological changes have steeply grown and, with them, the use of aging animal models. Mouse and rat models of aging, the most…

SenescenceRodentbiologysex differenceagingRC952-954.6PhysiologyGeneral MedicineDOENÇAS CARDIOVASCULARES EM ANIMALvascular dysfunctionmedicine.diseaseMenopausevascular agingvascular senescenceGeriatricsbiology.animalmedicineLife expectancyVascular agingEndothelial dysfunctionHormoneVascular senescence
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