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1. Full Text Resolvin D1 activates the inflammation resolving response at splenic and ventricular site following myocardial infarction leading to improved ventricular function
by Kain, Vasundhara and Ingle, Kevin A and Colas, Romain A and Dalli, Jesmond and Prabhu, Sumanth D and Serhan, Charles N and Joshi, Medha and Halade, Ganesh V
Journal of Molecular and Cellular Cardiology, ISSN 0022-2828, 2015, Volume 84, pp. 24 - 35
Abstract Unresolved inflammation is a major contributor to the development of heart failure following myocardial infarction (MI). Pro-resolving lipid... 
Cardiovascular | Myocardial infarction | Splenic remodeling | Resolution of inflammation | Metabololipidomics | Resolvin D1 | Neutrophils | SURVIVAL | CHRONIC HEART-FAILURE | PROTECTIVE ACTIONS | CARDIAC & CARDIOVASCULAR SYSTEMS | RESOLUTION | TISSUE | RECEPTOR | LIPID MEDIATORS | CELL BIOLOGY | THERAPY | PATHWAY | DISEASE | Cell Count | Male | Myocardial Infarction - diagnostic imaging | Spleen - drug effects | Extracellular Matrix - genetics | Inflammation - complications | Pulmonary Edema - physiopathology | Inflammation - drug therapy | Pulmonary Edema - complications | Receptors, Formyl Peptide - metabolism | Ultrasonography | Myocardial Infarction - physiopathology | Cell Polarity - drug effects | Spleen - pathology | Neutrophil Infiltration - drug effects | Ventricular Function - drug effects | Docosahexaenoic Acids - therapeutic use | Arachidonate 5-Lipoxygenase - metabolism | Docosahexaenoic Acids - chemistry | Extracellular Matrix - drug effects | Mice, Inbred C57BL | Cardiomegaly - diagnostic imaging | Cardiomegaly - drug therapy | Cardiomegaly - physiopathology | Pulmonary Edema - drug therapy | Cardiomegaly - complications | Collagen - metabolism | Docosahexaenoic Acids - pharmacology | Myocardial Infarction - complications | Macrophages - metabolism | Animals | Myocardial Infarction - drug therapy | Heart Ventricles - physiopathology | Prostaglandin-Endoperoxide Synthases - metabolism | Macrophages - drug effects | Ventricular Remodeling - drug effects | Heart Ventricles - drug effects | Inflammation | Heart attack | metabololipidomics | liposomes | myocardial infarction | splenic remodeling | neutrophils | resolution of inflammation
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2. Full Text Resolution of dilated cardiomyopathy in an adolescent with change of a failing highly active antiretroviral drug therapy
by Aliku, Twalib Olega and Lubega, Sulaiman and Lwabi, Peter
African Health Sciences, ISSN 1680-6905, 2015, Volume 15, Issue 1, pp. 288 - 292
Background: Cardiovascular dysfunction is a recognized complication of HIV infection in children. Cardiac complications of HIV usually occur late in the course... 
Dilated cardiomyopathy | HAART | MORTALITY | MEDICINE, GENERAL & INTERNAL | CARDIAC MORBIDITY | HUMAN-IMMUNODEFICIENCY-VIRUS | Dilated Cardiomyopathy | CHILDREN | Cardiomyopathy, Dilated - complications | Humans | Risk Factors | Ventricular Function, Left - drug effects | Antiretroviral Therapy, Highly Active - adverse effects | Cardiomegaly - diagnostic imaging | Ventricular Dysfunction, Left - etiology | Anticoagulants - therapeutic use | Treatment Outcome | CD4 Lymphocyte Count | Cardiomyopathy, Dilated - virology | Viral Load | Radiography | Medication Adherence | Ventricular Dysfunction, Left - drug therapy | Cardiomyopathy, Dilated - drug therapy | Adolescent | Counseling | HIV Infections - complications | Electrocardiography | Female | HIV Infections - drug therapy | Health and Medicine
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3. Full Text MicroRNAs in heart failure: from biomarker to target for therapy
by Vegter, Eline L and van der Meer, Peter and de Windt, Leon J and Pinto, Yigal M and Voors, Aiaan A
EUROPEAN JOURNAL OF HEART FAILURE, ISSN 1388-9842, 05/2016, Volume 18, Issue 5, pp. 457 - 468
MicroRNAs (miRNAs) are increasingly recognized to play important roles in cardiovascular diseases, including heart failure. These small, non-coding RNAs have... 
Heart failure | Antimir | MicroRNAs | Circulation | CIRCULATING MICRORNAS | FIBROSIS | CARDIAC & CARDIOVASCULAR SYSTEMS | SIGNATURES DIFFERENTIATE | HYPERTROPHY | ADULT HEARTS | CARDIAC RESYNCHRONIZATION THERAPY | EJECTION FRACTION | ACUTE MYOCARDIAL-INFARCTION | CARDIOVASCULAR-DISEASE | PLASMA MICRORNA | Biomarkers - metabolism | Acute Disease | Prognosis | Humans | Cardiomegaly - drug therapy | Heart Failure - physiopathology | Cardiomegaly - physiopathology | MicroRNAs - metabolism | Myocardium - pathology | Heart Failure - metabolism | Molecular Targeted Therapy | Heart Failure - drug therapy | Stroke Volume | Fibrosis | Chronic Disease | Cardiomegaly - metabolism
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4. Full Text Mechanism(s) of Systolic Blood Pressure Reduction and Drug Therapy in Hypertension
by Safar, Michel E
Hypertension, ISSN 0194-911X, 07/2007, Volume 50, Issue 1, pp. 167 - 171
C-REACTIVE PROTEIN | LOW-DOSE COMBINATION | METAANALYSIS | CONVERTING-ENZYME-INHIBITOR | ARTERIAL STIFFNESS | RESISTANCE ARTERIES | RENAL-FAILURE | PERIPHERAL VASCULAR DISEASE | LEFT-VENTRICULAR MASS | PULSE PRESSURE | CENTRAL AORTIC PRESSURE | Stroke - prevention & control | Kidney - drug effects | Humans | Cardiomegaly - etiology | Cardiomegaly - physiopathology | Hypertension - drug therapy | Systole | Antihypertensive Agents - therapeutic use | Remission Induction | Disease Progression | Hypertension - physiopathology | Animals | Arteries - physiopathology | Heart - drug effects | Hypertension - complications | Blood Pressure - drug effects | Kidney - physiopathology
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5. Full Text Genetic and pharmacologic hydrogen sulfide therapy attenuates ischemia-induced heart failure in mice
by Calvert, John W and Elston, Marah and Nicholson, Chad K and Gundewar, Susheel and Jha, Saurabh and Elrod, John W and Ramachandran, Arun and Lefer, David J
Circulation, ISSN 0009-7322, 07/2010, Volume 122, Issue 1, pp. 11 - 19
Background-Hydrogen sulfide (H2S) is an endogenous signaling molecule with potent cytoprotective effects. The present study evaluated the therapeutic potential... 
heart failure | OXIDATIVE STRESS | CARDIAC & CARDIOVASCULAR SYSTEMS | cystathionine gamma-Lyase | myocardial infarction | REPERFUSION INJURY | MYOCARDIAL ISCHEMIA/REPERFUSION INJURY | ischemia | PROTECTS | INFARCTION | REACTIVE OXYGEN | hydrogen sulfide | PHASE-2 ENZYMES | ENDOTHELIAL-CELLS | PERIPHERAL VASCULAR DISEASE | CARDIOPROTECTION | HEMATOLOGY | EXPRESSION | Myocardial Ischemia - genetics | Body Weight | Ventricular Function, Left - genetics | Male | Vasodilation - genetics | Ventricular Dysfunction, Left - genetics | Nuclear Respiratory Factor 1 - metabolism | Cystathionine gamma-Lyase - genetics | Heart Failure - etiology | Mice, Inbred C57BL | NF-E2-Related Factor 2 - drug effects | Organ Size | Heart Failure - genetics | Mice, Transgenic | Survival Rate | Sulfates - pharmacology | Cardiomegaly - enzymology | Nuclear Respiratory Factor 1 - drug effects | Heart Failure - drug therapy | Gene Expression Regulation, Enzymologic | Hydrogen Sulfide - therapeutic use | Animals | Cardiomegaly - prevention & control | Myocardial Ischemia - complications | NF-E2-Related Factor 2 - metabolism | Mice | Vasodilation - drug effects | Heart failure | Hydrogen sulfide | Animal experimentation | Care and treatment | Usage | Myocardial ischemia | Genetic aspects | Health aspects | cystathionine γ-Lyase
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6. Histone deacetylase: A potential therapeutic target for fibrotic disorders
by Pang, Maoyin and Zhuang, Shougang
Journal of Pharmacology and Experimental Therapeutics, ISSN 0022-3565, 11/2010, Volume 335, Issue 2, pp. 266 - 272
Histone deacetylases (HDACs) are enzymes that balance the acetylation activities of histone acetyltransferases on chromatin remodeling and play essential roles... 
FIBROBLAST ACTIVATION | CARDIAC-HYPERTROPHY | TRANSFORMING GROWTH-FACTOR-BETA-1 | INTERSTITIAL FIBROSIS | PHARMACOLOGY & PHARMACY | ANGIOTENSIN-II | CELL-PROLIFERATION | IDIOPATHIC PULMONARY-FIBROSIS | SYSTEMIC-SCLEROSIS | MYOFIBROBLASTIC DIFFERENTIATION | MYELOID METAPLASIA | Primary Myelofibrosis - drug therapy | Cystic Fibrosis - enzymology | Kidney Diseases - pathology | Humans | Cardiomegaly - drug therapy | Cystic Fibrosis - pathology | Scleroderma, Systemic - pathology | Kidney Diseases - drug therapy | Cardiomegaly - pathology | Histone Deacetylases - metabolism | Cardiomegaly - enzymology | Kidney Diseases - enzymology | Primary Myelofibrosis - pathology | Primary Myelofibrosis - enzymology | Scleroderma, Systemic - enzymology | Fibrosis | Idiopathic Pulmonary Fibrosis - pathology | Histone Deacetylase Inhibitors - therapeutic use | Idiopathic Pulmonary Fibrosis - enzymology | Cystic Fibrosis - drug therapy | Idiopathic Pulmonary Fibrosis - drug therapy | Scleroderma, Systemic - drug therapy
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7. Full Text GLP-1R Agonist Liraglutide Activates Cytoprotective Pathways and Improves Outcomes After Experimental Myocardial Infarction in Mice
by Mohammad Hossein Noyan-Ashraf and M. Abdul Momen and Kiwon Ban and Al-Muktafi Sadi and Yu-Qing Zhou and Ali M. Riazi and Laurie L. Baggio and R. Mark Henkelman and Mansoor Husain and Daniel J. Drucker
Diabetes, ISSN 0012-1797, 04/2009, Volume 58, Issue 4, pp. 975 - 983
GLP-1R Agonist Liraglutide Activates Cytoprotective Pathways and Improves Outcomes After Experimental Myocardial Infarction in Mice Mohammad Hossein... 
GLYCOGEN-SYNTHASE KINASE-3-BETA | ISCHEMIA-REPERFUSION INJURY | CARDIAC-FUNCTION | CONSCIOUS DOGS | ISCHEMIA/REPERFUSION INJURY | GLUCAGON-LIKE PEPTIDE-1 | ENDOCRINOLOGY & METABOLISM | RAT-HEART | DILATED CARDIOMYOPATHY | LEFT-VENTRICULAR PERFORMANCE | GLUCOSE-UPTAKE | Receptors, Glucagon - agonists | Heart - anatomy & histology | Body Weight | Glucagon-Like Peptide 1 - analogs & derivatives | Humans | Mice, Inbred C57BL | Organ Size | Cardiomegaly - pathology | Male | Diabetic Angiopathies - drug therapy | Animals | Myocardial Infarction - drug therapy | Glucagon-Like Peptide-1 Receptor | Mice | Blood Glucose - metabolism | Diabetes Mellitus, Type 2 - drug therapy | Liraglutide | Disease Models, Animal | Glucagon-Like Peptide 1 - therapeutic use | Type 2 diabetes | Hypoglycemic agents | Dosage and administration | Cellular signal transduction | Research | Drug therapy | Heart attack | Original
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8. Full Text Mitochondria-Targeted Antioxidant MitoQ10 Improves Endothelial Function and Attenuates Cardiac Hypertrophy
by Graham, Delyth and Huynh, Ngan N and Hamilton, Carlene A and Beattie, Elisabeth and Smith, Robin A.J and Cochemé, Helena M and Murphy, Michael P and Dominiczak, Anna F
Hypertension, ISSN 0194-911X, 08/2009, Volume 54, Issue 2, pp. 322 - 328
Mitochondria are a major site of reactive oxygen species production, which may contribute to the development of cardiovascular disease. Protecting mitochondria... 
Hypertension | Mitochondria | Endothelial function | Antioxidant | Hypertrophy | Rats, Inbred SHR | Risk Factors | Ubiquinone - analogs & derivatives | Cardiomegaly - drug therapy | Probability | Rats | Endothelium, Vascular - drug effects | Hypertension - drug therapy | Male | Antioxidants - pharmacology | Mitochondria - drug effects | Random Allocation | Membrane Potential, Mitochondrial - drug effects | Hypertension - physiopathology | Drug Delivery Systems | Ubiquinone - pharmacology | Animals | Cardiomegaly - prevention & control | Analysis of Variance | Sensitivity and Specificity | Blood Pressure - drug effects | Oxidative Stress - drug effects | Disease Models, Animal
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9. Full Text Signaling effectors underlying pathologic growth and remodeling of the heart
by Van Berlo, Jop H and Maillet, Marjorie and Molkentin, Jeffery D
Journal of Clinical Investigation, ISSN 0021-9738, 01/2013, Volume 123, Issue 1, pp. 37 - 45
Cardiovascular disease is the number one cause of mortality in the Western world. The heart responds to many cardiopathological conditions with hypertrophic... 
MEDICINE, RESEARCH & EXPERIMENTAL | HIGH-BLOOD-PRESSURE | MYOCARDIAL-INFARCTION | BETA-ADRENERGIC-RECEPTOR | IN-VIVO | KINASE-C-ALPHA | T-CELL LYMPHOMA | LEFT-VENTRICULAR MASS | PROTEIN PHOSPHATASE 2A | ENHANCES CARDIAC CONTRACTILITY | HISTONE DEACETYLASE | Arrhythmias, Cardiac - mortality | Humans | Heart Failure - physiopathology | Cardiomegaly - pathology | Arrhythmias, Cardiac - physiopathology | Arrhythmias, Cardiac - pathology | Ventricular Remodeling | Cardiomegaly - mortality | Heart Failure - etiology | Disease Models, Animal | Heart Failure - mortality | Arrhythmias, Cardiac - metabolism | Death, Sudden - epidemiology | Signal Transduction | Cardiomegaly - drug therapy | Cardiomegaly - physiopathology | Arrhythmias, Cardiac - etiology | Clinical Trials as Topic | Heart Failure - metabolism | Heart Failure - pathology | Cardiomegaly - complications | Heart Failure - drug therapy | Arrhythmias, Cardiac - drug therapy | Animals | Cardiomegaly - metabolism | Heart | Physiological aspects | Care and treatment | Cardiovascular diseases | Health aspects | Risk factors | Review Series
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10. Full Text Combination of angiotensin-(1-7) with perindopril is better than single therapy in ameliorating diabetic cardiomyopathy
by Hao, Panpan and Yang, Jianmin and Liu, Yanping and Zhang, Mingxiang and Zhang, Kai and Gao, Fei and Chen, Yuguo and Zhang, Cheng and Zhang, Yun
Scientific Reports, ISSN 2045-2322, 2015, Volume 5, Issue 1, p. 8794
We recently found that overexpression of angiotensin (Ang)-converting enzyme 2, which metabolizes Ang-II to Ang-(1-7) and Ang-I to Ang-(1-9), may improve left... 
ACTIVATION | MYOCARDIAL FIBROSIS | MULTIDISCIPLINARY SCIENCES | CARDIAC-HYPERTROPHY | HIGH GLUCOSE | PROXIMAL TUBULAR CELLS | RECEPTOR MAS | DEFICIENT MICE | DYSFUNCTION | RAT MODEL | FIBROBLASTS | Receptors, Angiotensin - metabolism | Diabetic Cardiomyopathies - metabolism | Diabetic Cardiomyopathies - drug therapy | Apoptosis - drug effects | Transforming Growth Factor beta1 - metabolism | Cardiomegaly - etiology | Cardiomegaly - pathology | Male | Peptide Fragments - pharmacology | Perindopril - administration & dosage | Perindopril - pharmacology | Heart Ventricles - ultrastructure | Peptidyl-Dipeptidase A - metabolism | Angiotensin I - pharmacology | Collagen - biosynthesis | p38 Mitogen-Activated Protein Kinases - metabolism | Phosphorylation - drug effects | Drug Therapy, Combination | Heart Ventricles - pathology | Disease Models, Animal | Fibroblasts - metabolism | Echocardiography | Peptide Fragments - administration & dosage | Angiotensin I - administration & dosage | Cardiomegaly - drug therapy | Rats | Diabetic Cardiomyopathies - diagnosis | Ventricular Dysfunction, Left - prevention & control | Blood Glucose - drug effects | Animals | Ventricular Dysfunction, Left - drug therapy | Mitogen-Activated Protein Kinase 3 - metabolism | Cell Differentiation - drug effects | Fibroblasts - drug effects | Cell Communication - drug effects | Fibrosis | Cell Proliferation - drug effects | Fibroblasts - cytology | Hemodynamics - drug effects | Oxidative Stress - drug effects | Heart Ventricles - drug effects | Mitogen-Activated Protein Kinase 1 - metabolism | Heart | Enzymes | Cardiomyopathy | Diabetes mellitus | Rodents | Angiotensin | Diabetes | Ventricle | Angiotensin II | Hypertrophy | Apoptosis
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11. Full Text Cardiac Metabolism and its Interactions With Contraction, Growth, and Survival of Cardiomyocytes
by Kolwicz, Stephen C and Purohit, Suneet and Tian, Rong
Circulation Research, ISSN 0009-7330, 08/2013, Volume 113, Issue 5, pp. 603 - 616
The network for cardiac fuel metabolism contains intricate sets of interacting pathways that result in both ATP-producing and non–ATP-producing end points for... 
metabolic signaling | cardiac pathology | cardiac metabolism | metabolic therapy | CHRONIC HEART-FAILURE | CARDIAC & CARDIOVASCULAR SYSTEMS | PENTOSE-PHOSPHATE PATHWAY | MYOCARDIAL SUBSTRATE METABOLISM | LEFT-VENTRICULAR PERFORMANCE | COENZYME-A DECARBOXYLASE | DIET-INDUCED OBESITY | ACTIVATED-RECEPTOR-ALPHA | MUSCLE PROTEIN-SYNTHESIS | GLUCAGON-LIKE PEPTIDE-1 | FATTY-ACID OXIDATION | PERIPHERAL VASCULAR DISEASE | HEMATOLOGY | Adaptation, Physiological | Fatty Acids - adverse effects | Phosphorylation | Mitochondria, Heart - metabolism | Fatty Acids - therapeutic use | Humans | Myocardial Contraction - physiology | Substrate Specificity | Mitochondria, Heart - drug effects | Autophagy | Adenosine Triphosphate - metabolism | Myocardium - metabolism | TOR Serine-Threonine Kinases - physiology | Heart Failure - diet therapy | Fatty Acids - metabolism | Myocytes, Cardiac - cytology | Cell Survival | Heart - growth & development | Insulin Resistance | Diabetes Mellitus - metabolism | Heart Failure - metabolism | Heart Failure - drug therapy | Obesity - metabolism | Randomized Controlled Trials as Topic | Animals | Diet | Energy Metabolism | Myocytes, Cardiac - metabolism | Protein Processing, Post-Translational | Metabolic Networks and Pathways - drug effects | Apoptosis | Cardiomegaly - metabolism
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12. Full Text Sitagliptin Reduces Cardiac Apoptosis, Hypertrophy and Fibrosis Primarily by Insulin-Dependent Mechanisms in Experimental type-II Diabetes. Potential Roles of GLP-1 Isoforms
by Picatoste, Belén and Ramírez, Elisa and Caro-Vadillo, Alicia and Iborra, Cristian and Egido, Jesús and Tuñón, José and Lorenzo, Óscar
PLoS ONE, ISSN 1932-6203, 10/2013, Volume 8, Issue 10, p. e78330
Background: Myocardial fibrosis is a key process in diabetic cardiomyopathy. However, their underlying mechanisms have not been elucidated, leading to a lack... 
HEART | CELLS | ACTIVATION | DPP-4 INHIBITION | GLUCAGON-LIKE PEPTIDE-1 | MYOCARDIAL-INFARCTION | RAT | MULTIDISCIPLINARY SCIENCES | GENE-EXPRESSION | RECEPTOR | IMPROVES | Diabetic Cardiomyopathies - metabolism | Metformin - therapeutic use | Diabetic Cardiomyopathies - drug therapy | Insulin - physiology | Fibroblasts - physiology | Cardiomegaly - etiology | Glucagon-Like Peptide 1 - physiology | Male | Pyrazines - therapeutic use | Diabetes Mellitus, Type 2 - metabolism | Cardiotonic Agents - therapeutic use | Glucose Intolerance - drug therapy | Sitagliptin Phosphate | Drug Evaluation, Preclinical | Diabetes Mellitus, Type 2 - complications | Disease Models, Animal | Triazoles - therapeutic use | Hypoglycemic Agents - therapeutic use | Metformin - pharmacology | Cardiomegaly - drug therapy | Cells, Cultured | Glucagon-Like Peptide 1 - pharmacology | Rats | Myocardium - pathology | Cardiotonic Agents - pharmacology | Fibronectins - metabolism | Protein Isoforms - physiology | Hypoglycemic Agents - pharmacology | Protein Isoforms - pharmacology | Triazoles - pharmacology | Animals | Myocytes, Cardiac - drug effects | Myocytes, Cardiac - physiology | Fibrosis | PPAR delta - metabolism | Diabetes Mellitus, Type 2 - drug therapy | Pyrazines - pharmacology | Apoptosis | Cardiomegaly - metabolism | Hyperglycemia | Glucagon | Heart enlargement | Glucose | Insulin | Dextrose | Diabetes therapy | Heart | Plasma | Heart attacks | Peptides | Cardiomyopathy | Deceleration | Cardiovascular disease | Kinases | Palmitic acid | Eutrophication | Proteins | Rodents | Fibroblasts | Extracellular matrix | Heart diseases | Glucagon-like peptide 1 | Heart failure | Cell survival | Hyperlipidemia | Diabetes mellitus | Cardiomyocytes | Metabolism | Signaling | Cell death | Isoforms | Metformin | Diabetes | Laboratory animals | Hypertrophy | Structure-function relationships
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