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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

6

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

7

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

8

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

9

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

10

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

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