نتائج البحث

1

Angiopoietin-1 enhanced myocyte mitosis, engraftment, and the reparability of hiPSC-CMs for treatment of myocardial infarction

المؤلفون: Jianyi Zhang, Xin Chen, Shu Uin Gan, Lei Ye, Szejie Loo, Shihua Tan, Zhonghao Tao, Liping Su, Guizhen Tee

المصدر: Cardiovascular Research. 117:1578-1591

الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::e27ddb2fb8d4cc740f38ba6ac88669a3Test
https://doi.org/10.1093/cvr/cvaa215Test

2

Yap is required for scar formation but not myocyte proliferation during heart regeneration in zebrafish

المؤلفون: Brooke E Jeffery, Michael A. Flinn, Brian A. Link, Caitlin C. O'Meara

المصدر: Cardiovascular Research. 115:570-577

مصطلحات موضوعية: 0301 basic medicine, Physiology, Heart growth, 030204 cardiovascular system & hematology, Biology, Animals, Genetically Modified, Cicatrix, 03 medical and health sciences, 0302 clinical medicine, Physiology (medical), Animals, Regeneration, Myocyte, Myocytes, Cardiac, Zebrafish, Cells, Cultured, Cell Proliferation, Gene knockdown, Ventricular Remodeling, Heart development, Macrophages, Regeneration (biology), YAP-Signaling Proteins, Fibroblasts, Zebrafish Proteins, biology.organism_classification, Fibrosis, Hedgehog signaling pathway, Rats, Cell biology, Cold Temperature, Disease Models, Animal, 030104 developmental biology, Gene Expression Regulation, Heart Injuries, Trans-Activators, Apoptosis Regulatory Proteins, Cardiology and Cardiovascular Medicine, Myofibroblast, Signal Transduction

الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::1ea5128266dc160d2fb09091e65588d3Test
https://doi.org/10.1093/cvr/cvy243Test

3

Loss of AKAP150 promotes pathological remodelling and heart failure propensity by disrupting calcium cycling and contractile reserve

المؤلفون: Haifeng Yin, Jing Li, L. Fernando Santana, Yi Chen, Stephen W. Luckey, Merle L. Gilbert, Xiaoyun Guo, Lei Li, G. Stanley McKnight, John D. Scott, Qinghang Liu, Benjamin M.L. Drum

المصدر: Cardiovascular research, vol 113, iss 2
Li, L; Li, J; Drum, BM; Chen, Y; Yin, H; Guo, X; et al.(2017). Loss of AKAP150 promotes pathological remodelling and heart failure propensity by disrupting calcium cycling and contractile reserve. Cardiovascular Research, 113(2), 147-159. doi: 10.1093/cvr/cvw221. UC Davis: Retrieved from: http://www.escholarship.org/uc/item/0912z16qTest

مصطلحات موضوعية: 0301 basic medicine, Time Factors, Physiology, Myocardial Ischemia, A Kinase Anchor Proteins, Cardiorespiratory Medicine and Haematology, Cardiovascular, Contractility, Rats, Sprague-Dawley, Mice, AKAP150, Pathological remodelling, Dilated, 2.1 Biological and endogenous factors, Ventricular Function, Myocyte, Myocytes, Cardiac, Myocardial infarction, Aetiology, Cells, Cultured, Mice, Knockout, Cultured, Ventricular Remodeling, Calcineurin, Cardiac myocyte, Dilated cardiomyopathy, Phospholamban, Sarcoplasmic Reticulum, Cardiac hypertrophy, Heart Disease, Phenotype, Cardiology, RNA Interference, Cardiology and Cardiovascular Medicine, Cardiac, Cardiomyopathy, Dilated, medicine.medical_specialty, Cardiomyopathy, Cells, Knockout, Myocardial Reperfusion Injury, Heart failure, Biology, Transfection, Sarcoplasmic Reticulum Calcium-Transporting ATPases, 03 medical and health sciences, Physiology (medical), Internal medicine, medicine, Animals, Genetic Predisposition to Disease, Calcium Signaling, Heart Failure, Pressure overload, Myocytes, NFATC Transcription Factors, Animal, Calcium-Binding Proteins, Isoproterenol, Ryanodine Receptor Calcium Release Channel, Original Articles, medicine.disease, Fibrosis, Rats, Disease Models, Animal, 030104 developmental biology, Endocrinology, Cardiovascular System & Hematology, Disease Models, Sprague-Dawley

وصف الملف: application/pdf

الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::ed411433a7cd22b2f8adb9f95e09c1c8Test
https://doi.org/10.1093/cvr/cvw221Test

4

Reg proteins direct accumulation of functionally distinct macrophage subsets after myocardial infarction

المؤلفون: Henning Warnecke, Jochen Pöling, Julia Detzer, Praveen Gajawada, Juan M. Adrian-Segarra, Holger Lörchner, Thomas Braun, Jennifer Kulhei, Hans W.M. Niessen, Stefan Günther, Yunlong Hou

المساهمون: Cardio-thoracic surgery, Pathology, ACS - Heart failure & arrhythmias

المصدر: Lörchner, H, Hou, Y, Adrian-Segarra, J M, Kulhei, J, Detzer, J, Günther, S, Gajawada, P, Warnecke, H, Niessen, H W, Pöling, J & Braun, T 2018, ' Reg proteins direct accumulation of functionally distinct macrophage subsets after myocardial infarction ', Cardiovascular Research, vol. 114, no. 12, pp. 1667-1679 . https://doi.org/10.1093/cvr/cvy126Test
Cardiovascular Research, 114(12), 1667-1679. Oxford University Press

مصطلحات موضوعية: Male, 0301 basic medicine, Physiology, Myocardial Infarction, Pancreatitis-Associated Proteins, Biology, Cell Line, Flow cytometry, Rats, Sprague-Dawley, Mice, 03 medical and health sciences, Physiology (medical), Gene expression, medicine, Animals, Antigens, Ly, Humans, Myocyte, Macrophage, Myocytes, Cardiac, Myocardial infarction, Mice, Knockout, Regulation of gene expression, Oncostatin M Receptor beta Subunit, medicine.diagnostic_test, Chemotaxis, Macrophages, Histocompatibility Antigens Class II, Editorials, medicine.disease, Neoplasm Proteins, Cell biology, Mice, Inbred C57BL, Disease Models, Animal, Phenotype, 030104 developmental biology, Gene Expression Regulation, Cell culture, Signal transduction, Cardiology and Cardiovascular Medicine, Signal Transduction

الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::048aec616927908bac9a9411c44303deTest
https://doi.org/10.1093/cvr/cvy126Test

5

Reactivation of the Nkx2.5 cardiac enhancer after myocardial infarction does not presage myogenesis

المصدر: Cardiovascular Research. 114:1098-1114

مصطلحات موضوعية: 0301 basic medicine, Time Factors, Physiology, Cellular differentiation, Cell Plasticity, Population, Myocardial Infarction, Mice, Transgenic, Biology, Muscle Development, Stem cell marker, Epigenesis, Genetic, 03 medical and health sciences, Physiology (medical), Animals, Regeneration, Myocyte, Myocytes, Cardiac, Progenitor cell, education, Cells, Cultured, education.field_of_study, Ventricular Remodeling, Myogenesis, Stem Cells, Cell Differentiation, Original Articles, Chromatin Assembly and Disassembly, Embryonic stem cell, Cell biology, Mice, Inbred C57BL, Disease Models, Animal, Enhancer Elements, Genetic, Phenotype, 030104 developmental biology, Homeobox Protein Nkx-2.5, Stem cell, Transcriptome, Cardiology and Cardiovascular Medicine, Signal Transduction

الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::37875f984255347e38e52ff2d07404eeTest
https://doi.org/10.1093/cvr/cvy069Test

6

Endogenous Sonic Hedgehog limits inflammation and angiogenesis in the ischaemic skeletal muscle of mice

المؤلفون: Annabel Reynaud, Caroline Caradu, Chloé James, Alexandre Guy, Marie-Ange Renault, Alain-Pierre Gadeau

المساهمون: Biologie des maladies cardiovasculaires = Biology of Cardiovascular Diseases, Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Bordeaux (UB)-Centre National de la Recherche Scientifique (CNRS), Boullé, Christelle, Université de Bordeaux (UB)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)

المصدر: Cardiovascular Research
Cardiovascular Research, Oxford University Press (OUP), 2018, 114 (5), pp.759-770. ⟨10.1093/cvr/cvy017⟩
Cardiovascular Research, 2018, 114 (5), pp.759-770. ⟨10.1093/cvr/cvy017⟩

مصطلحات موضوعية: Vascular Endothelial Growth Factor A, 0301 basic medicine, Time Factors, animal structures, Physiology, Angiogenesis, Myoblasts, Skeletal, Neovascularization, Physiologic, endothelial cells 2, Biology, MyoD, 03 medical and health sciences, [SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular system, Ischemia, Physiology (medical), medicine, Animals, Myocyte, Hedgehog Proteins, Sonic hedgehog, Muscle, Skeletal, Hedgehog, Inflammation, Mice, Knockout, Myogenesis, Chemotaxis, Macrophages, Skeletal muscle, [SDV.MHEP.CSC] Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular system, Hindlimb, Cell biology, Disease Models, Animal, Sonic Hedgehog, 030104 developmental biology, medicine.anatomical_structure, Article RECHERCHE, Regional Blood Flow, embryonic structures, biology.protein, Chemokines, Cardiology and Cardiovascular Medicine, Smoothened, Blood Flow Velocity, Signal Transduction

وصف الملف: application/pdf

الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::ea8f112c0f15edc5f37a32838e50e200Test
https://doi.org/10.1093/cvr/cvy017Test

7

Elevated plasma catecholamines functionally compensate for the reduced myogenic tone in smooth muscle STIM1 knockout mice but with deleterious cardiac effects

المؤلفون: Prahalathan Pichavaram, Salvatore Mancarella, Kirk W. Evanson, Jonathan H. Jaggar, Wen Yin

المصدر: Cardiovascular Research. 114:668-678

مصطلحات موضوعية: inorganic chemicals, 0301 basic medicine, Cardiac function curve, medicine.medical_specialty, Sympathetic Nervous System, Heart Diseases, Physiology, Myocytes, Smooth Muscle, Blood Pressure, Muscle, Smooth, Vascular, 03 medical and health sciences, Catecholamines, Heart Rate, Physiology (medical), Internal medicine, medicine, Prazosin, Animals, Myocyte, Stromal Interaction Molecule 1, Phenylephrine, Cells, Cultured, Mice, Knockout, biology, Chemistry, Myocardium, Heart, Original Articles, Vinculin, Fibrosis, Up-Regulation, Actin Cytoskeleton, 030104 developmental biology, Endocrinology, Vasoconstriction, Knockout mouse, biology.protein, Catecholamine, medicine.symptom, Cardiology and Cardiovascular Medicine, Signal Transduction, medicine.drug

الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::04a4b7abb73129f2bd4e748ee249f545Test
https://doi.org/10.1093/cvr/cvy015Test

8

From genetics to response to injury: vascular smooth muscle cells in aneurysms and dissections of the ascending aorta

المؤلفون: Jean-Baptiste Michel, Guillaume Jondeau, Dianna M. Milewicz

المصدر: Cardiovascular Research. 114:578-589

مصطلحات موضوعية: 0301 basic medicine, Vascular smooth muscle, Physiology, Myocytes, Smooth Muscle, Aorta, Thoracic, Context (language use), Vascular Remodeling, 030204 cardiovascular system & hematology, Biology, Muscle, Smooth, Vascular, Extracellular matrix, 03 medical and health sciences, Aortic aneurysm, 0302 clinical medicine, Aneurysm, Risk Factors, Physiology (medical), medicine.artery, medicine, Animals, Humans, Myocyte, Thoracic aorta, Genetic Predisposition to Disease, Aorta, Aortic Aneurysm, Thoracic, medicine.disease, Extracellular Matrix, Cell biology, Invited Spotlight Reviews, Disease Models, Animal, Phenotype, 030104 developmental biology, cardiovascular system, Cardiology and Cardiovascular Medicine, Dilatation, Pathologic, Peptide Hydrolases, Signal Transduction

الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::95d79bc2ccfe94fa633183b4190adfc3Test
https://doi.org/10.1093/cvr/cvy006Test

9

Luma is not essential for murine cardiac development and function

المؤلفون: Kirk L. Peterson, Yusu Gu, Xi Fang, Matthew J. Stroud, William H. Bradford, Larry Gerace, Nuno Guimarães-Camboa, Sylvia M. Evans, Nancy D. Dalton, Ju Chen, Jianlin Zhang, Jennifer Veevers

المصدر: Stroud, M J, Fang, X, Zhang, J, Guimaraes-Camboa, N, Veevers, J, Dalton, N D, Gu, Y, Bradford, W H, Peterson, K L, Evans, S M, Gerace, L & Chen, J 2018, ' Luma is not essential for murine cardiac development and function ', Cardiovascular Research, vol. 114, no. 3, pp. 378-388 . https://doi.org/10.1093/cvr/cvx205Test

مصطلحات موضوعية: Male, 0301 basic medicine, Physiology, LINC complex, Myocytes, Smooth Muscle, Luma, Cardiomyopathy, Linker of nucleoskeleton to cytoskeleton complex, Biology, medicine.disease_cause, Mechanotransduction, Cellular, Nuclear envelope, Germline, 03 medical and health sciences, 0302 clinical medicine, Physiology (medical), Morphogenesis, medicine, Animals, Humans, Myocyte, Genetic Predisposition to Disease, Myocytes, Cardiac, Nuclear Matrix, Arrhythmogenic Right Ventricular Dysplasia, Cells, Cultured, Cytoskeleton, Mice, Knockout, Pressure overload, Mutation, Heart development, Myocardium, Editorials, Gene Expression Regulation, Developmental, Membrane Proteins, Outer nuclear membrane, Heart, Fibroblasts, medicine.disease, Cell biology, Mice, Inbred C57BL, 030104 developmental biology, Inner nuclear membrane, Female, Hypertrophy, Left Ventricular, Arrhythmogenic right ventricular cardiomyopathy, Cardiology and Cardiovascular Medicine, 030217 neurology & neurosurgery

وصف الملف: application/pdf

الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::06d20eebd07ad7e81236802d474f827bTest
https://doi.org/10.1093/cvr/cvx205Test

10

The expression of the rare caveolin-3 variant T78M alters cardiac ion channels function and membrane excitability

المؤلفون: Mirko Baruscotti, Elena Vezzoli, Dario DiFrancesco, Giulia Campostrini, Lia Crotti, Alessio Lissoni, Maura Francolini, Peter J. Schwartz, Claudia Bazzini, Riccardo Cappato, Annalisa Bucchi, Stefano Severi, Matteo Fantini, Mattia Bonzanni, Andrea Barbuti, Ilaria Rivolta, Raffaella Milanesi

المساهمون: Campostrini, Giulia, Bonzanni, Mattia, Lissoni, Alessio, Bazzini, Claudia, Milanesi, Raffaella, Vezzoli, Elena, Francolini, Maura, Baruscotti, Mirko, Bucchi, Annalisa, Rivolta, Ilaria, Fantini, Matteo, Severi, Stefano, Cappato, Riccardo, Crotti, Lia, Schwartz, Peter J., DiFrancesco, Dario, Barbuti, Andrea, Campostrini, G, Bonzanni, M, Lissoni, A, Bazzini, C, Milanesi, R, Vezzoli, E, Francolini, M, Baruscotti, M, Bucchi, A, Rivolta, I, Fantini, M, Severi, S, Cappato, R, Crotti, L, Schwartz, P, Di Francesco, D, Barbuti, A

المصدر: Cardiovascular Research
CARDIOVASCULAR RESEARCH

مصطلحات موضوعية: 0301 basic medicine, Potassium Channels, Caveolin 3, Physiology, Caveolin 1, Genetic disease, PROTEIN, Action Potentials, Muscle Proteins, 030204 cardiovascular system & hematology, Rats, Sprague-Dawley, Mice, 0302 clinical medicine, BIO/09 - FISIOLOGIA, EXOME DATA, Heart Rate, Caveolin, Medicine and Health Sciences, Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels, Myocyte, Myocytes, Cardiac, Mice, Knockout, Models, Cardiovascular, LOCALIZATION, 3T3 Cells, Electrophysiology, Ion channels, cardiovascular system, Ion Channels and Arrhythmias, Ion channel, Cardiology and Cardiovascular Medicine, Ion Channel Gating, Arrhythmia, Genetic diseases, LONG-QT SYNDROME, Biology, MYOCYTES, Caveolae, Transfection, LATE SODIUM CURRENT, Kv1.5 Potassium Channel, 03 medical and health sciences, Physiology (medical), INFANT-DEATH-SYNDROME, Animals, Humans, HCN4, Computer Simulation, Transcription factor, MUTATIONS, Cardiac arrhythmia, Arrhythmias, Cardiac, MED/11 - MALATTIE DELL'APPARATO CARDIOVASCOLARE, Original Articles, Fibroblasts, Myocardial Contraction, CHRONIC ATRIAL-FIBRILLATION, Kinetics, 030104 developmental biology, Membrane protein, Mutation, Neuroscience

وصف الملف: STAMPA; application/pdf

الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::6b0fbeb746b9e11b23fcf7054b1a0cd1Test
https://doi.org/10.1093/cvr/cvx122Test

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