Search results for "Cardiac"

showing 10 items of 1495 documents

Deregulation of TLR4 signaling pathway characterizes Bicuspid Aortic valve syndrome

2019

AbstractBicuspid aortic valve (BAV) disease is recognized to be a syndrome with a complex and multifaceted pathophysiology. Its progression is modulated by diverse evolutionary conserved pathways, such as Notch-1 pathway. Emerging evidence is also highlighting the key role of TLR4 signaling pathway in the aortic valve pathologies and their related complications, such as sporadic ascending aorta aneurysms (AAA). Consistent with these observations, we aimed to evaluate the role of TLR4 pathway in both BAV disease and its common complication, such as AAA. To this aim, 70 subjects with BAV (M/F 50/20; mean age: 58.8 ± 14.8 years) and 70 subjects with tricuspid aortic valve (TAV) (M/F 35/35; mea…

Male0301 basic medicineAortic valveBicuspid Aortic valve syndromeHeart Valve Diseaseslcsh:MedicineDisease0302 clinical medicineBicuspid aortic valveBicuspid Aortic Valve DiseaseTLR4lcsh:ScienceAortaAged 80 and overMultidisciplinarySyndromeMiddle AgedPathophysiologymedicine.anatomical_structureAortic Valvecardiovascular systemCardiologyFemaleSignal Transductionmedicine.medical_specialtyCardiologyArticleProinflammatory cytokine03 medical and health sciencesmedicine.arteryInternal medicineAscending aortamedicineHumansbicuspid valveAgedbicuspid valve; TLR4; aortic diseaseBAV TLR4 AAATumor Necrosis Factor-alphabusiness.industryInterleukinslcsh:RSettore MED/23 - Chirurgia CardiacaValvular diseaseaortic diseasemedicine.diseaseToll-Like Receptor 4030104 developmental biologyTLR4lcsh:QbusinessComplication030217 neurology & neurosurgeryScientific Reports
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Deregulation of Notch1 pathway and circulating endothelial progenitor cell (EPC) number in patients with bicuspid aortic valve with and without ascen…

2018

AbstractBicuspid aortic valve (BAV) is frequently associated with the development of ascending aortic aneurysm, even if the underlying mechanisms remain to be clarified. Here, we investigated if a deregulation of Notch1 signaling pathway and endothelial progenitor cells (EPCs) number is associated with BAV disease and an early ascending aortic aneurysm (AAA) onset. For this purpose, 70 subjects with BAV (M/F 50/20; mean age: 58.8 ± 14.8 years) and 70 subjects with tricuspid aortic valve (TAV) (M/F 35/35; mean age: 69.1 ± 12.8 years) and AAA complicated or not, were included. Interestingly, patients with AAA showed a significant increase in circulating Notch1 levels and EPC number than subje…

Male0301 basic medicineAortic valveNotch1 signaling pathwatHeart Valve Diseases030204 cardiovascular system & hematologyAortic aneurysm0302 clinical medicineBicuspid aortic valveBicuspid Aortic Valve DiseaseNotch Signaling Pathwaycirculating EPC populationsReceptor Notch1ReceptorAortaEndothelial Progenitor CellsAged 80 and overMultidisciplinaryQRMiddle AgedAortic Aneurysmmedicine.anatomical_structureAortic Valvecardiovascular systemCardiologyMedicineFemaleTricuspid ValveSignal TransductionAdultmedicine.medical_specialtyBicuspid aortic valveEndothelial Progenitor Cells (EPC)ScienceNotch signaling pathwayBicuspid Aortic Valve (BAV)Endothelial progenitor cellArticleBicuspid aortic valve; Notch1 signaling pathwat; ascending aortic aneurysm03 medical and health sciencesascending aortic aneurysmInternal medicinemedicineHumansIn patientcardiovascular diseasesProgenitor cellNotch 1 signaling pathwayAgedTricuspid Aortic Valve (TAV)Ascending Aorta Aneurysm (AAA)business.industrySettore MED/23 - Chirurgia Cardiacamedicine.disease030104 developmental biologybusiness
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Systemic blockade of ACVR2B ligands attenuates muscle wasting in ischemic heart failure without compromising cardiac function

2020

Signaling through activin receptors regulates skeletal muscle mass and activin receptor 2B (ACVR2B) ligands are also suggested to participate in myocardial infarction (MI) pathology in the heart. In this study, we determined the effect of systemic blockade of ACVR2B ligands on cardiac function in experimental MI, and defined its efficacy to revert muscle wasting in ischemic heart failure (HF). Mice were treated with soluble ACVR2B decoy receptor (ACVR2B-Fc) to study its effect on post-MI cardiac remodeling and on later HF. Cardiac function was determined with echocardiography, and myocardium analyzed with histological and biochemical methods for hypertrophy and fibrosis. Pharmacological blo…

Male0301 basic medicineCardiac function curvemedicine.medical_specialtyActivin Receptors Type IIMyocardial IschemiaMyostatinBiochemistryMuscle hypertrophyMice03 medical and health sciences0302 clinical medicineInternal medicineGeneticsmedicineAnimalsMyocyteMyocardial infarctionMolecular BiologyVentricular Remodelingbiologybusiness.industrySkeletal muscleHeartmedicine.disease3. Good healthBlockadeMice Inbred C57BLDisease Models AnimalMuscular Atrophy030104 developmental biologymedicine.anatomical_structureCardiologybiology.proteinbusiness030217 neurology & neurosurgeryACVR2BSignal TransductionTranscription FactorsBiotechnologyThe FASEB Journal
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Cross-Sectional Associations between Homoarginine, Intermediate Phenotypes, and Atrial Fibrillation in the Community—The Gutenberg Health Study

2018

Homoarginine has come into the focus of interest as a biomarker for cardiovascular disease. Atrial fibrillation (AF) causes a substantial increase in morbidity and mortality. Whether circulating homoarginine is associated with occurrence or persistence of AF and may serve as a new predictive biomarker remains unknown. We measured plasma levels of homoarginine in the population-based Gutenberg health study (3761 patients included, of them 51.7% males), mean age 55.6 &plusmn

Male0301 basic medicineCardiac function curvemedicine.medical_specialtyPopulationlcsh:QR1-502030204 cardiovascular system & hematologyBiochemistryArticlelcsh:MicrobiologyElectrocardiography03 medical and health sciences0302 clinical medicineResidence CharacteristicsRisk FactorsInterquartile rangeInternal medicinemedicineHumanshomoarginineatrial fibrillationpopulation-based cohortRisk factoreducationMolecular BiologyAgededucation.field_of_studybusiness.industryAtrial fibrillationOdds ratioMiddle Agedmedicine.diseaseHealth SurveysConfidence interval3. Good healthdiastolic disfunctionCross-Sectional StudiesPhenotype030104 developmental biologyCase-Control StudiesCardiologyBiomarker (medicine)biomarkerFemalebusinessBiomolecules
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Telmisartan cardioprotects from the ischaemic/hypoxic damage through a miR‐1‐dependent pathway

2019

The aim of this study was to investigate whether telmisartan protects the heart from the ischaemia/reperfusion damage through a local microRNA-1 modulation. Studies on the myocardial ischaemia/reperfusion injury in vivo and on the cardiomyocyte hypoxia/reoxygenation damage in vitro were done. In vivo, male Sprague-Dawley rats administered for 3 weeks with telmisartan 12 mg/kg/d by gastric gavage underwent ischaemia/reperfusion of the left descending coronary artery. In these rats, infarct size measurement, ELISA, immunohistochemistry (IHC) and reverse transcriptase real-time polymerase chain reaction showed that expressions of connexin 43, potassium voltage-gated channel subfamily Q member …

Male0301 basic medicineCell SurvivalMyocardial InfarctionIschemiaConnexinMyocardial Reperfusion InjuryPharmacologymiR‐1telmisartanCell Lineconnexin 43Rats Sprague-Dawleyhypoxic H9c2 cells03 medical and health sciences0302 clinical medicineIn vivomedicineAnimalsBcl-2Myocytes CardiacKCNQ1ChemistryBcl‐2Original ArticlesCell BiologyTransfectionHypoxia (medical)medicine.diseasemiR-1Cell HypoxiaIn vitroRatsMicroRNAsmyocardial ischaemia/reperfusion030104 developmental biologyProto-Oncogene Proteins c-bcl-2030220 oncology & carcinogenesisKCNQ1 Potassium ChannelMolecular Medicinehypoxic H9c2 cellOriginal Articlemedicine.symptomTelmisartanReperfusion injurymedicine.drugJournal of Cellular and Molecular Medicine
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KCND3 potassium channel gene variant confers susceptibility to electrocardiographic early repolarization pattern

2019

BACKGROUND: The presence of an early repolarization pattern (ERP) on the surface ECG is associated with risk of ventricular fibrillation and sudden cardiac death. Family studies have shown that ERP is a highly heritable trait, but molecular genetic determinants are unknown. METHODS: To identify genetic susceptibility loci for ERP, we performed a GWAS and meta-analysis in 2,181 cases and 23,641 controls of European ancestry. RESULTS: We identified a genome-wide significant (P < 5 × 10(–8)) locus in the potassium voltage-gated channel subfamily D member 3 (KCND3) gene that was successfully replicated in additional 1,124 cases and 12,510 controls. A subsequent joint meta-analysis of the discov…

Male0301 basic medicineGenotypeHeart VentriclesGenome-wide association studyLocus (genetics)BiologyPolymorphism Single NucleotideWhite PeopleSudden cardiac deathElectrocardiography03 medical and health sciences0302 clinical medicineGenetic variationmedicineGenetic predispositionHumansSNPGWASGenetic Predisposition to DiseaseJ-POINT ELEVATIONS422LAlleleGENOME-WIDE ASSOCIATIONGeneMUTATIONAllelesMETAANALYSISGeneticsGeneral Medicinemedicine.diseaseddc:Death Sudden CardiacShal Potassium Channels030104 developmental biologyGenetic Loci030220 oncology & carcinogenesisVentricular FibrillationCORONARY-ARTERY-DISEASEFemaleVENTRICULAR-FIBRILLATIONClinical MedicineTranscriptomeGenome-Wide Association Study
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Relationships of growth factors, proinflammatory cytokines, and anti-inflammatory cytokines with long-term clinical results of autologous bone marrow…

2017

Aim The aim of the study was to test the hypothesis suggesting that the pre-intervention levels of proinflammatory cytokines, anti-inflammatory cytokines, and angiogenic growth factors predict the long-term clinical results of autologous bone marrow-derived mononuclear cell (ABMMC) transplantation in patients with primary ST elevation myocardial infarction (STEMI). Methods and results From 2003 to 2006, a total of 62 patients with primary STEMI were enrolled in an open randomized study registered under the title ESTABOMA. Patients were randomized into two groups: group 1 included patients treated with percutaneous coronary intervention (PCI) and ABMMC transplantation (n = 28); group 2 compr…

Male0301 basic medicinePhysiologyCardiovascular ProceduresCell Transplantationmedicine.medical_treatmentMyocardial InfarctionSocial Scienceslcsh:Medicine030204 cardiovascular system & hematologyPathology and Laboratory MedicineVascular MedicineGastroenterologyAnginaEndocrinology0302 clinical medicineImmune PhysiologyMedicine and Health SciencesBlood and Lymphatic System ProceduresPsychologyMyocardial infarctionlcsh:ScienceImmune ResponseBone Marrow TransplantationInnate Immune SystemMultidisciplinaryCardiac TransplantationAnginaMiddle AgedBrain natriuretic peptidesurgical procedures operativeCytokinesIntercellular Signaling Peptides and ProteinsFemaleInflammation MediatorsResearch Articlemedicine.medical_specialtySocial PsychologyImmunologyCardiologySurgical and Invasive Medical ProceduresTransplantation AutologousProinflammatory cytokine03 medical and health sciencesSigns and SymptomsDiagnostic MedicineGrowth FactorsInternal medicineчрескожное коронарное вмешательствоmedicineHumanscardiovascular diseasesInflammationTransplantationEndocrine Physiologybusiness.industrylcsh:RBiology and Life SciencesPercutaneous coronary interventionOrgan TransplantationMolecular Developmentmedicine.diseaseпровоспалительные цитокиныинфаркт миокардаTransplantation030104 developmental biologyImmune SystemHeart failureImmunologyConventional PCIтрансплантация мононуклеарных клетокlcsh:Qbusinessаутологичная трансплантация костного мозгаDevelopmental BiologyStem Cell Transplantation
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Investigating and re-evaluating the role of glycogen synthase kinase 3 beta kinase as a molecular target for cardioprotection by using novel pharmaco…

2019

Aims Glycogen synthase kinase 3 beta (GSK3β) link with the mitochondrial Permeability Transition Pore (mPTP) in cardioprotection is debated. We investigated the role of GSK3β in ischaemia (I)/reperfusion (R) injury using pharmacological tools. Methods and results Infarct size using the GSK3β inhibitor BIO (6-bromoindirubin-3'-oxime) and several novel analogues (MLS2776-MLS2779) was determined in anaesthetized rabbits and mice. In myocardial tissue GSK3β inhibition and the specificity of the compounds was tested. The mechanism of protection focused on autophagy-related proteins. GSK3β localization was determined in subsarcolemmal (SSM) and interfibrillar mitochondria (IFM) isolated from Lang…

Male0301 basic medicinePhysiologyMyocardial InfarctionAutophagy-Related ProteinsMyocardial Reperfusion Injury030204 cardiovascular system & hematologyMitochondrionPharmacologyMitochondrial Membrane Transport ProteinsMitochondria HeartStructure-Activity Relationship03 medical and health scienceschemistry.chemical_compound0302 clinical medicineReperfusion therapyPhysiology (medical)AnimalsMyocytes CardiacProtein Kinase InhibitorsGSK3BMice Knockoutchemistry.chemical_classificationCardioprotectionReactive oxygen speciesGlycogen Synthase Kinase 3 betaMolecular StructureMitochondrial Permeability Transition PoreChemistryKinaseMPTPIsolated Heart PreparationMice Inbred C57BLDisease Models Animal030104 developmental biologyMitochondrial permeability transition poreFemaleRabbitsCardiology and Cardiovascular MedicineCyclophilin DSignal TransductionCardiovascular Research
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Stable Oxidative Cytosine Modifications Accumulate in Cardiac Mesenchymal Cells From Type2 Diabetes Patients

2018

Rationale: Human cardiac mesenchymal cells (CMSCs) are a therapeutically relevant primary cell population. Diabetes mellitus compromises CMSC function as consequence of metabolic alterations and incorporation of stable epigenetic changes. Objective: To investigate the role of α-ketoglutarate (αKG) in the epimetabolic control of DNA demethylation in CMSCs. Methods and Results: Quantitative global analysis, methylated and hydroxymethylated DNA sequencing, and gene-specific GC methylation detection revealed an accumulation of 5-methylcytosine, 5-hydroxymethylcytosine, and 5-formylcytosine in the genomic DNA of human CMSCs isolated from diabetic donors. Whole heart genomic DNA analysis reveale…

Male0301 basic medicinePhysiologyPopulationheartBiologyMixed Function OxygenasesCytosineMice03 medical and health sciencesProto-Oncogene ProteinsfibroblastsHuman Umbilical Vein Endothelial CellsAnimalsHumansMyocytes CardiacEpigeneticsEnzyme InhibitorseducationCells CulturedEpigenomicsDemethylationeducation.field_of_studyDNA methylationDNA methylation; epigenomics; fibroblasts; heart; hyperglycemia; metabolism; physiology; cardiology and cardiovascular medicineMesenchymal Stem CellsSettore MED/13 - ENDOCRINOLOGIABase excision repairMolecular biologyThymine DNA GlycosylaseMice Inbred C57BLHEK293 Cells030104 developmental biologyDNA demethylationDiabetes Mellitus Type 2epigenomicsDNA methylationKetoglutaric AcidshyperglycemiaThymine-DNA glycosylaseCardiology and Cardiovascular MedicineOxidation-ReductionmetabolismCirculation Research
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Immunity, Inflammation and Heart Failure. Their Role on Cardiac Function and Iron Status

2019

Aims: Heart failure is a clinical syndrome characterized by subclinical systemic inflammation and immune system activation associated with iron deficiency. No data exist on the various activations of immune-mediated mechanisms of inflammation in heart failure patients with reduced/preserved ejection fraction. We aimed to (1) investigate possible differences in inflammatory parameters and oxidative stress, and (2) detect a different iron status between groups. Materials and Methods: We enrolled 50 consecutive Caucasian outpatients with heart failure. All patients underwent echocardiographic measurements, laboratory determinations, evaluation of iron status and Toll-like receptors, and NF-κB …

Male0301 basic medicineheart failureSystemic inflammationGastroenterologyVentricular Function LeftElectrocardiographychemistry.chemical_compound0302 clinical medicineiron deficiencyImmunology and Allergyejection fraction; heart failure; inflammation; iron deficiency; toll-like receptorejection fractionOriginal ResearchAged 80 and overEjection fractionbiologymedicine.diagnostic_testToll-Like ReceptorsIron deficiencyMiddle AgedHeart Function TestsSerum ironCytokinesFemaleDisease SusceptibilityInflammation Mediatorsmedicine.symptomlcsh:Immunologic diseases. AllergyCardiac function curvemedicine.medical_specialtyIronImmunology03 medical and health sciencesHepcidinsInternal medicinemedicineHumansAgedCreatininebusiness.industryImmunitymedicine.diseaseFerritinOxidative Stress030104 developmental biologychemistryinflammationHeart failurebiology.proteintoll-like receptorlcsh:RC581-607businessBiomarkers030215 immunology
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