Search results for "mouse heart"

showing 5 items of 5 documents

Nerves projecting from the intrinsic cardiac ganglia of the pulmonary veins modulate sinoatrial node pacemaker function

2013

Rationale: Autonomic nerves from sinoatrial node (SAN) ganglia are known to regulate SAN function. However, it is unclear whether remote pulmonary vein ganglia (PVG) also modulate SAN pacemaker rhythm. Objective: To investigate whether in the mouse heart PVG modulate SAN function. Methods and Results: In hearts from 45 C57BL and 7 Connexin40+/GFP mice, we used tyrosine-hydroxylase (TH) and choline-acetyltransferase (ChAT) immunofluorescence labeling to characterize adrenergic and cholinergic elements, repectively, within the PVG and SAN. PVG project postganglionic nerves to the SAN. TH and ChAT stained nerves, enter the SAN as an extensive, dense mesh-like neural network. Neurons in PVG are…

Malemedicine.medical_specialtysinoatrial nodepulmonary veinsPhysiologyAdrenergicMice TransgenicStimulationIn Vitro TechniquesMiceFetal HeartBiological ClocksHeart Conduction SystemHeart RatePhysiology (medical)Internal medicineAtrial FibrillationHeart ratemouse heartmedicineAnimalsHumansSinus rhythmIntrinsic cardiac gangliaSinoatrial NodeSinoatrial nodebusiness.industryOriginal ArticlesMiddle AgedElectric StimulationElectrophysiological PhenomenaMice Inbred C57BLoptical mappingAtropinemedicine.anatomical_structureEndocrinologyPulmonary Veinscardiac arrhythmiasCatheter AblationCardiologyCholinergicFemaleGangliaElectrical conduction system of the heartCardiology and Cardiovascular Medicinebusinessmedicine.drugCardiovascular Research
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VEGF-B-induced vascular growth leads to metabolic reprogramming and ischemia resistance in the heart

2014

Abstract Angiogenic growth factors have recently been linked to tissue metabolism. We have used genetic gain‐ and loss‐of function models to elucidate the effects and mechanisms of action of vascular endothelial growth factor‐B (VEGF‐B) in the heart. A cardiomyocyte‐specific VEGF‐B transgene induced an expanded coronary arterial tree and reprogramming of cardiomyocyte metabolism. This was associated with protection against myocardial infarction and preservation of mitochondrial complex I function upon ischemia‐reperfusion. VEGF‐B increased VEGF signals via VEGF receptor‐2 to activate Erk1/2, which resulted in vascular growth. Akt and mTORC1 pathways were upregulated and AMPK downregulated, …

VEGF‐Bmedicine.medical_specialtyMedicine (General)AngiogenesiseducationMOUSE HEARTIschemiaVEGF-B610 Medicine & healthmTORC1ischemiaBiologyQH426-470CONTRIBUTESchemistry.chemical_compoundangiogenesisR5-920CARDIAC-FUNCTIONInternal medicinemedicineGeneticsFAILUREta318Myocardial infarctionFATTY-ACID UPTAKEREPERFUSION INJURY610 Medicine & healthProtein kinase BMYOCARDIAL HYPERTROPHYAMPKta3121medicine.diseaseCell biologyARTERIOGENESISVascular endothelial growth factorMICEEndocrinologychemistry3121 General medicine internal medicine and other clinical medicineendothelial cellMolecular Medicine3111 BiomedicineReperfusion injurymetabolism
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Molecular factors involved in the angiogenesis process of exercised mouse hearts

2008

angiogenesis mouse hearts
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Dissimilar effects of doxorubicin and isoproterenol on morphology, H2O2 content and catalase activity in mouse heart

1988

PharmacologyCardiotoxicityMorphology (linguistics)biologyCatalaseChemistrybiology.proteinmedicineDoxorubicinPharmacologyMouse Heartmedicine.drugPharmacological Research Communications
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“Pro-youthful” factors in the “labyrinth” of cardiac rejuvenation

2016

IF 3.350; International audience; The mechanisms of aging and senescence include various endogenous and exogenous factors. Among cardiovascular diseases, heart failure is a typical age-related disease. New strategies to restore cardiomyocyte cells have been reported: endogenous substances that can regenerate the heart's cardiomyocytes have been described: follistatin like 1 (FSTL1), growth-differentiation factor 11 (GDF11) and insulin-like growth factor 1 (IGF-I). Manipulation of the different anti and pro-pathways is essential to discover new approaches to regenerative therapies. (C) 2016 Elsevier Inc. All rights reserved.

0301 basic medicineAgingStem-Cellsmedicine.medical_treatmentEndogenyCardiovascular-DiseaseBioinformaticsBiochemistryEndocrinologyFollistatin-Like 1Myocytes CardiacInsulin-Like Growth Factor Ibiology[SDV.MHEP.GEG]Life Sciences [q-bio]/Human health and pathology/Geriatry and gerontologyGrowth differentiation factorGrowth-Factor-I3. Good healthIGF-IGrowth Differentiation FactorsBone Morphogenetic ProteinsCardiacMouse HeartSenescencemedicine.medical_specialtyFollistatin-Related ProteinsGene-Expression[ SDV.MHEP.GEG ] Life Sciences [q-bio]/Human health and pathology/Geriatry and gerontologyFSTL1Mammalian Heart03 medical and health sciencesMyocardial-InfarctionInternal medicineGeneticsmedicineHumansRegenerationRejuvenationMolecular BiologyHeart FailureYoung BloodTelomerase ExpressionRegeneration (biology)Growth factorCell Biologymedicine.disease030104 developmental biologyEndocrinologyHeart failureGDF11GDF11biology.proteinFollistatin
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