Search results for " STRESS"

showing 10 items of 3936 documents

miR-133a Enhances the Protective Capacity of Cardiac Progenitors Cells after Myocardial Infarction

2014

Summary miR-133a and miR-1 are known as muscle-specific microRNAs that are involved in cardiac development and pathophysiology. We have shown that both miR-1 and miR-133a are early and progressively upregulated during in vitro cardiac differentiation of adult cardiac progenitor cells (CPCs), but only miR-133a expression was enhanced under in vitro oxidative stress. miR-1 was demonstrated to favor differentiation of CPCs, whereas miR-133a overexpression protected CPCs against cell death, targeting, among others, the proapoptotic genes Bim and Bmf. miR-133a-CPCs clearly improved cardiac function in a rat myocardial infarction model by reducing fibrosis and hypertrophy and increasing vasculari…

Cardiac function curveProgrammed cell deathMyocardial InfarctionGene ExpressionCardiomegalyBiologyBiochemistryArticleMuscle hypertrophyParacrine signallingDownregulation and upregulationmiR-133a; Cardiac Progenitors Cells; Myocardial InfarctionFibrosisREGENERATIONmicroRNAGeneticsmedicineMyocyteAnimalsRNA MessengerOXIDATIVE STRESSlcsh:QH301-705.5ENGINEERED HEART-TISSUElcsh:R5-920Gene Expression ProfilingMICRORNAComputational BiologyCell BiologyMUSCLEmedicine.disease3. Good healthCell biologyRatsAPOPTOSISHYPERTROPHYMicroRNAsDIFFERENTIATIONlcsh:Biology (General)ImmunologyGROWTHRNA Interferencelcsh:Medicine (General)EMBRYONIC STEM-CELLSMyoblasts CardiacDevelopmental BiologyStem Cell Reports
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Doxorubicin induces wide-spread transcriptional changes in the myocardium of hearts distinguishing between mice with preserved and impaired cardiac f…

2021

Abstract Aims Doxorubicin (DOX) is an important drug for the treatment of various tumor entities. However, the occurrence of heart failure limits its application. This study investigated differential gene expression profiles in the left and right ventricles of DOX treated mice with either preserved or impaired myocardial function. We provide new mechanistic insights into the pathophysiology of DOX-induced heart failure and have discovered pathways that counteract DOX-induced cardiotoxicity. Main methods We used in total 48 male mice and applied a chronic low dose DOX administration (5 mg/kg per injection, in total 20 mg/kg over 4 weeks) to induce heart failure. Echocardiographic parameters …

Cardiac function curveTranscription GeneticPharmacologymedicine.disease_causeGeneral Biochemistry Genetics and Molecular BiologyElectrocardiographypolycyclic compoundsmedicineAnimalsCluster AnalysisDoxorubicinGeneral Pharmacology Toxicology and Pharmaceuticschemistry.chemical_classificationReactive oxygen speciesCardiotoxicitybusiness.industryGene Expression ProfilingMyocardiumGeneral Medicinemedicine.diseasePathophysiologyMice Inbred C57BLGene expression profilingOxidative StresschemistryDoxorubicinHeart failureHeart Function TestsbusinessOxidative stressmedicine.drugLife Sciences
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Iron overload does not potentiate doxorubicin induced cardiotoxicity in vivo in mice and in vitro in cardiomyocytes cell cultures

2013

Background: Doxorubicin (DOX), an anticancer anthracycline, is known to induce serious cardiotoxicity, which is believed to be mediated by oxidative stress and complex interactions with iron. However, the relations between iron metabolism and DOX-induced cardiotoxicity remain a matter of controversy. Methods: Firstly, we used an in vivo murine model of iron overloading (IO) where male C57BL/6 mice received during 3 weeks (D0-D20) a daily dextran-iron injection (15 mg/kg/day.) and then (D21) a single dose of 6 mg/kg DOX. We evaluated cardiac function with echocardiography, myocardial gene's expression, nitro-oxidative stress levels and iron status. Secondly, the anti-proliferative activity o…

Cardiac function curvemedicine.medical_specialtyCardiotoxicityAnthracyclinebusiness.industrymedicine.disease_causeEndocrinologyAtrial natriuretic peptideIn vivoInternal medicinepolycyclic compoundsmedicineDoxorubicinViability assayCardiology and Cardiovascular MedicinebusinessOxidative stressmedicine.drugEuropean Heart Journal
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0132 : Oxidative stress and cardio-metabolic alterations induced by postnatal programming can be reversed in adulthood by a short-term moderate calor…

2016

Postnatal overfeeding (PNOF) in rodents induces early programming of cardio-metabolic risk. Our aim was to determine if a moderate diet restriction could restore cardio-metabolic alterations induced by PNOF. Immediately after birth, litters of C57BL/6 mice were either maintained at 9 (normal litter, NL), or reduced to 3 (small litter, SL) to induce PNOF. At weaning, all mice received a standard diet ad libitum (AL). At 6 month of age, half of the NL and SL mice were assigned to a moderate 20% calorie restriction (CR: NLCR, SLCR) for one month, while the other mice continued to eat AL (AL: NLAL, SLAL). Glucose and insulin tolerance tests, cardiac function (echocardiography), body composition…

Cardiac function curvemedicine.medical_specialtyEjection fractionbiologybusiness.industryCalorie restrictionCarbohydrate metabolismmedicine.disease_causemedicine.diseaseInsulin receptorEndocrinologyInsulin resistanceInternal medicinemedicinebiology.proteinWeaningbusinessCardiology and Cardiovascular MedicineOxidative stressArchives of Cardiovascular Diseases Supplements
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Impact of intra-aortic balloon counterpulsation on all-cause mortality among patients with Takotsubo syndrome complicated by cardiogenic shock: resul…

2023

Abstract Aims Takotsubo syndrome (TTS) is an acute and reversible left ventricular dysfunction and can be complicated by cardiogenic shock (CS). However, few data are available on optimal care in TTS complicated by CS. Aim of this study was to evaluate short- and long-term impact of intra-aortic balloon pumping (IABP) on mortality in this setting. Methods and results In a multi-centre, international registry on TTS, 2248 consecutive patients were enrolled from 38 centres from Germany, Italy, and Spain. Of the 2248 patients, 212 (9.4%) experienced CS. Patients with CS had a higher prevalence of diabetes (27% vs. 19%), male sex (25% vs. 10%), and right ventricular involvement (10% vs. 5%) (P …

Cardiogenic shock GEIST IABP In-hospital complications Intra-aortic balloon counter-pulsation Stress cardiomyopathy Takotsubo syndrome
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Mechanisms of Increased Vascular Superoxide Production in an Experimental Model of Idiopathic Dilated Cardiomyopathy

2005

Objective— In the present study, we sought to identify mechanisms underlying increased oxidative stress in vascular tissue in an experimental animal model of chronic congestive heart failure (CHF). Methods and Results— Superoxide and nitric oxide (NO) was measured in vessels from cardiomyopathic hamsters (CHF hamsters) and golden Syrian hamsters. We also determined expression of endothelial nitric oxide synthase (NOSIII), the soluble guanylyl cyclase, the cGMP-dependent kinase, and the NADPH oxidase. To analyze the contribution of the renin-angiotensin system to oxidative stress, CHF hamsters were treated with the angiotensin-converting enzyme inhibitor captopril for 200 days (120 mg · kg …

Cardiomyopathy DilatedMalemedicine.medical_specialtyCaptoprilNitric Oxide Synthase Type IIIReceptors Cytoplasmic and NuclearAngiotensin-Converting Enzyme InhibitorsNitric Oxidemedicine.disease_causeNitric oxideRenin-Angiotensin Systemchemistry.chemical_compoundSoluble Guanylyl CyclaseSuperoxidesCricetinaeInternal medicineIdiopathic dilated cardiomyopathymedicineAnimalsHeart FailureNADPH oxidaseMesocricetusbiologybusiness.industrySuperoxideMyocardiumBody WeightMicrofilament ProteinsNADPH OxidasesCaptoprilOrgan SizePhosphoproteinsDisease Models AnimalOxidative StressEndocrinologychemistryGuanylate CyclaseACE inhibitorbiology.proteinFemaleCardiology and Cardiovascular MedicinebusinessSoluble guanylyl cyclaseCell Adhesion MoleculesOxidative stressmedicine.drugArteriosclerosis, Thrombosis, and Vascular Biology
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C022 Experimental approaches of oxidative stress and cardiotoxicity associated with anthracyclines administration

2009

The chronic cardiotoxicity of anthracyclines anticancer drugs is one of the main factors which limits their prolonged use. Clinically, this cardiotoxicity results in a cardiomyopathy with irreversible congestive heart failure with high mortality. The molecular mechanisms, which could explain this cardiac toxicity, are complex but seem distinct from the anticancer mechanism. Several hypotheses were advanced, but it appears that the production of reactive oxygen and nitrogen species (RONS) constitutes the common denominator.In a first study, we evaluated the acute effect of epirubicin administration on the evolution of cardiac functional parameters and production of RONS. Isolated perfused ra…

CardiotoxicityChemotherapybusiness.industrymedicine.medical_treatmentCardiomyopathyGeneral MedicinePharmacologymedicine.diseasemedicine.disease_causeHeart failureAnesthesiamedicineDoxorubicinCardioprotective AgentCardiology and Cardiovascular MedicinebusinessOxidative stressmedicine.drugEpirubicinArchives of Cardiovascular Diseases
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Cardioprotection by gene therapy: A review paper on behalf of the Working Group on Drug Cardiotoxicity and Cardioprotection of the Italian Society of…

2015

Ischemic heart disease remains the leading cause of death worldwide. Ischemic pre-, post-, and remote conditionings trigger endogenous cardioprotection that renders the heart resistant to ischemic-reperfusion injury (IRI). Mimicking endogenous cardioprotection by modulating genes involved in cardioprotective signal transduction provides an opportunity to reproduce endogenous cardioprotection with better possibilities of translation into the clinical setting. Genes and signaling pathways by which conditioning maneuvers exert their effects on the heart are partially understood. This is due to the targeted approach that allowed identifying one or a few genes associated with IRI and cardioprote…

CardiotoxinIschemic heart diseaseCardiologyMyocardial IschemiaPreconditioningMyocardial Reperfusion InjuryCardioprotectionRemote conditioningCardiotoxinsPostconditioningGene therapyMedicalHumansMyocardialIschemic PreconditioningSocieties MedicalCardioprotection; Gene therapy; Genomics; Ischemic heart disease; Postconditioning; Preconditioning; Remote conditioning; Cardiology; Cardiotoxicity; Cardiotoxins; Gene Targeting; Genetic Therapy; Humans; Ischemic Preconditioning Myocardial; Italy; Myocardial Ischemia; Myocardial Reperfusion Injury; Oxidative Stress; Societies MedicalCardioprotection; Gene therapy; Genomics; Ischemic heart disease; Postconditioning; Preconditioning; Remote conditioning; Cardiology; Cardiotoxicity; Cardiotoxins; Gene Targeting; Genetic Therapy; Humans; Ischemic Preconditioning; Myocardial; Italy; Myocardial Ischemia; Myocardial Reperfusion Injury; Oxidative Stress; Societies; Medical; Cardiology and Cardiovascular MedicineOxidative StreGenomicsGenetic TherapyCardioprotection Gene therapy Genomics Ischemic heart disease Postconditioning Preconditioning Remote conditioningCardiotoxicityOxidative StressCardioprotection; Gene therapy; Genomics; Ischemic heart disease; Postconditioning; Preconditioning; Remote conditioningItalyIschemic Preconditioning MyocardialGene TargetingGenomicSocietiesCardiology and Cardiovascular MedicineHuman
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Current and emerging drugs for the treatment of atherosclerosis: the evidence to date

2022

Introduction: Atherosclerosis can be considered a chronic inflammatory process that stands out as a dominant cause of cardiovascular disease (CVD). Since blood lipids are the leading risk factor for atherosclerosis development, lowering low-density lipoprotein cholesterol (LDL-C) and other apolipoprotein B-containing lipoproteins reduces the risk of future cardiovascular events. However, there has been significant progress in developing lipid-lowering drugs for aggressive management of dyslipidemia, the rates of CVD events remain unacceptably high, so there is great need to identify novel therapeutic pathways targeting the atherosclerosis process.Areas covered: We discussed the current guid…

Cardiovascular DiseasesInternal MedicineHumansCholesterol LDLAtherosclerosis cardiovascular disease inflammation oxidative stress preventionGeneral MedicineAtherosclerosisOxidantsCardiology and Cardiovascular MedicineLipidsDyslipidemiasExpert Review of Cardiovascular Therapy
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From molecular mechanisms to clinical management of antineoplastic drug-induced cardiovascular toxicity: A translational overview

2019

Significance: Antineoplastic therapies have significantly improved the prognosis of oncology patients. However, these treatments can bring to a higher incidence of side-effects, including the worrying cardiovascular toxicity (CTX). Recent Advances: Substantial evidence indicates multiple mechanisms of CTX, with redox mechanisms playing a key role. Recent data singled out mitochondria as key targets for antineoplastic drug-induced CTX; understanding the underlying mechanisms is, therefore, crucial for effective cardioprotection, without compromising the efficacy of anti-cancer treatments. Critical Issues: CTX can occur within a few days or many years after treatment. Type I CTX is associated…

Cardiovascular toxicityPhysiologymedicine.medical_treatmentAntineoplastic drugClinical BiochemistryAntineoplastic Agents030204 cardiovascular system & hematologyPharmacologyBiochemistryCardiac cellcancer immunotherapy; chemotherapy; ErbB2 inhibitors; oxidative/nitrosative stress; tyrosine kinase inhibitors; vascular endothelial growth factor; Antineoplastic Agents; Cardiotoxicity; Humans; Mitochondria; Oxidation-Reduction03 medical and health scienceschemistry.chemical_compoundErbB2 inhibitors cancer immunotherapy chemotherapy oxidative/nitrosative stress tyrosine kinase inhibitors vascular endothelial growth factor0302 clinical medicinetyrosine kinase inhibitorcancer immunotherapy; chemotherapy; ErbB2 inhibitors; oxidative/nitrosative stress; tyrosine kinase inhibitors; vascular endothelial growth factorChemotherapy; ErbB2 inhibitors; vascular endothelial growth factor; tyrosine kinase inhibitors; oxidative/nitrosative stress; cancer immunotherapyCancer immunotherapytyrosine kinase inhibitorsmedicineHumansChemotherapyMolecular BiologyGeneral Environmental ScienceCardioprotectionComprehensive Invited ReviewsChemotherapyErbB2 inhibitorcancer immunotherapyvascular endothelial growth factorbusiness.industryCell BiologyCardiotoxicityMitochondriaVascular endothelial growth factoroxidative/nitrosative streErbB2 inhibitorschemistry030220 oncology & carcinogenesisGeneral Earth and Planetary SciencesbusinessOxidation-ReductionAfter treatmentoxidative/nitrosative stress
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