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Satellite Glial Cell Activation and Sympathetic Imbalance in Cardiomyopathy and Arrhythmias
Organization UNIVERSITY OF CALIFORNIA LOS ANGELESLocation LOS ANGELES, UNITED STATESPosted 1 Apr 2022Deadline 31 Mar 2026 โ ๏ธ
NIHUS FederalResearch GrantFY2025AblationAnimalsArrhythmiaAstroproteinAttenuatedCalcium Ion SignalingCalcium SignalingCardiacCardiac ArrhythmiaCardiac DiseasesCardiac DisordersCardiac infarctionCardiomyopathiesCatecholaminesCause of DeathCell Communication and SignalingCell SignalingCervicothoracic GanglionChronicChronic DiseaseChronic IllnessCommunicating JunctionCommunicationCongestive CardiomyopathyConnexin 43Connexin43Cx43DataDevelopmentDilated CardiomyopathyDiseaseDisorderDrugsDysfunctionElectrophysiologyElectrophysiology (science)FibrosisFunctional disorderFutureG Protein-Complex ReceptorG Protein-Coupled Receptor GenesG-Protein-Coupled ReceptorsGFA-ProteinGFAPGPCRGap JunctionsGeneticGliaGlial CellsGlial Fibrillary Acid ProteinGlial Fibrillary Acidic ProteinGlial Intermediate Filament ProteinGoalsHealthHeartHeart ArrhythmiasHeart DiseasesHeart InjuriesHeart failureHumanHyperactivityInflammatoryInflammatory Bowel DiseasesInflammatory Bowel DisorderInjuryIntracellular Communication and SignalingInvestigatorsIschemiaKolliker's reticulumLV remodelingLeft Ventricular DysfunctionLeft Ventricular RemodelingLevarterenolLevonorepinephrineLinkLow-resistance JunctionMediatingMedicalMedicationMiceMice MammalsModelingModern ManMorphologyMurineMusMyocardial DiseasesMyocardial DisorderMyocardial InfarctMyocardial InfarctionMyocardiopathiesMyocardiumNerve CellsNerve Impulse TransmissionNerve TransmissionNerve UnitNervous SystemNeural CellNeurocyteNeurogliaNeuroglial CellsNeurologic Body SystemNeurologic Organ SystemNeuronal DysfunctionNeuronal TransmissionNeuronsNeurophysiology / ElectrophysiologyNexus JunctionNon-neuronal cellNonneuronal cellNoradrenalineNorepinephrinePatientsPharmaceutical PreparationsPhysiopathologyPlayPreventionProcessPurinesReperfusion TherapyResearch PersonnelResearchersRoleSignal TransductionSignal Transduction SystemsSignalingSignaling MoleculeStellate GangliasStellate GanglionStructure of stellate ganglionSupporting CellSympathetic GangliaSympathinsSynapsesSynapticTechniquesTestingTherapeuticTransgenic MiceUpregulationVentricular ArrhythmiaVentricular TachycardiaViralattenuateattenuatesaxon signalingaxon-glial signalingaxonal signalingbeta-adrenergic receptorbiological signal transductioncardiac failurecardiac infarctcardiac injurycardiac musclecell typechronic disorderchronic paincoronary attackcoronary infarctcoronary infarctioncytokinedeath riskdevelopmentaldrug/agentelectrophysiologicalglia signalingglial activationglial cell activationglial signalingheart attackheart disorderheart infarctheart infarctionheart musclehuman datahuman modelinflammatory disease of the intestineinflammatory disorder of the intestineinhibitorinjuriesinjury to organsintestinal autoinflammationleft ventricle abnormalityleft ventricle remodelingmodel of humanmortalitymortality riskmouse modelmultidisciplinarymurine modelmyocardium diseasemyocardium disordernerve cementnerve signalingneuralneural controlneural dysfunctionneural regulationneural signalingneurochemicalneurochemistryneuromodulationneuromodulatoryneuronalneuronal excitabilityneuronal signalingneuroregulationneurotransmissionnovelorgan injurypathophysiologypig modelpiglet modelporcine modelpreventpreventingrelease factorreperfusionside effectsocial roleswine modelsynapsetargeted drug therapytargeted drug treatmentstargeted therapeutictargeted therapeutic agentstargeted therapytargeted treatmenttherapeutic targettoolฮฒ-adrenergic receptor
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Description preview
PROJECT SUMMARY/ABSTRACT
Cardiac injury predisposes patients to heart failure (HF), and ventricular tachycardia/fibrillation (VT/VF).
Development of HF and VT/VF after cardiac injury is tightly linked to sympathetic neural remodeling. Although
several medications targeting cardiac sympathetic excess reduce mortality following cardiac injury,โฆ
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