Cardiac hypertrophy and fibrosis

Regular dark chocolate consumption may insulate your heart against cardiac dysfunction: Chocolate-derived compound theobromine-based adjunct therapy for cardiac hypertrophy and fibrosis: Theobromine,  one of the main components of dark chocolate, decreases Mir-29 expression, activates Wnt- signaling and its components GSK3B, ICAT/CTNNBIP1, HBP1, and GLIS2, attenuates pathologic hypertrophy, inhibits fibrosis of the heart tissue, and improves cardiac function via upregulation of its target gene, 4/September/2018, 1.42 am
Regular dark chocolate consumption may insulate your heart against cardiac dysfunction: Chocolate-derived compound theobromine-based adjunct therapy for cardiac hypertrophy and fibrosis: Theobromine,  one of the main components of dark chocolate, decreases Mir-29 expression, activates Wnt- signaling and its components GSK3B, ICAT/CTNNBIP1, HBP1, and GLIS2, attenuates pathologic hypertrophy, inhibits fibrosis of the heart tissue, and improves cardiac function via upregulation of its target gene, 4/September/2018, 1.42 am 960 720 Dr Boomi's Genom-2-Discovery Center

Introduction: What they say:   A recent study from the Institute of Pharmacology and Toxicology, Technical University Munich (TUM), 80802, Munich, Germany; DZHK (German Center for Cardiovascular Research), partner site Munich…

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A sere(ne)laxin-way to stay free of cardiac diseases: Serelaxin-based therapy for attenuating pathogenesis-associated with Myocardial infarction: Serelaxin, a recombinant Relaxin-2,  decreases IRF3 (Interferon regulatory transcription factor-3), GM-CSF (Granulocyte-macrophage colony-stimulating factor) and GRK2(G protein-coupled receptor kinase) expression, inhibits undue leucocyte activation and invasion, suppresses recruitment of inflammatory cells, inhibits ventricular dilation, and promotes heart repair and survival, via up-regulation of its target gene, 27/August/2018, 11.25 pm
A sere(ne)laxin-way to stay free of cardiac diseases: Serelaxin-based therapy for attenuating pathogenesis-associated with Myocardial infarction: Serelaxin, a recombinant Relaxin-2,  decreases IRF3 (Interferon regulatory transcription factor-3), GM-CSF (Granulocyte-macrophage colony-stimulating factor) and GRK2(G protein-coupled receptor kinase) expression, inhibits undue leucocyte activation and invasion, suppresses recruitment of inflammatory cells, inhibits ventricular dilation, and promotes heart repair and survival, via up-regulation of its target gene, 27/August/2018, 11.25 pm 960 720 Dr Boomi's Genom-2-Discovery Center

Introduction: What they say: A recent study from Department of Systems Biology, Harvard Medical School, Boston, Massachusetts, USA; and Cardiovascular Research Center, Massachusetts General Hospital and Harvard Medical School, Boston,…

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Serelaxin (SLX)-based therapy for cardiomyocyte proliferation and heart regeneration: Serelaxin (SLX), a recombinant relaxin-2, decreases tumor suppressor MiR-128 and cyclin-dependent kinase inhibitor p27 expression, increases SUZ12 expression, increases Cyclin E and CDK2 expression, promotes proliferation/re-entry of postnatal/adult cardiomyocytes, attenuates fibrosis, ameliorates cardiac dysfunction, and promotes heart repair in response to myocardial infarction, via up-regulation of its target gene, 26/August/2018, 7.10 pm
Serelaxin (SLX)-based therapy for cardiomyocyte proliferation and heart regeneration: Serelaxin (SLX), a recombinant relaxin-2, decreases tumor suppressor MiR-128 and cyclin-dependent kinase inhibitor p27 expression, increases SUZ12 expression, increases Cyclin E and CDK2 expression, promotes proliferation/re-entry of postnatal/adult cardiomyocytes, attenuates fibrosis, ameliorates cardiac dysfunction, and promotes heart repair in response to myocardial infarction, via up-regulation of its target gene, 26/August/2018, 7.10 pm 960 720 Dr Boomi's Genom-2-Discovery Center

Introduction: What they say: A recent study from Department of Pathology and Laboratory Medicine, University of Cincinnati College of Medicine, Cincinnati, OH, 45267, USA; Key Laboratory of Molecular Target and…

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Serelaxin (SLX)-based therapy for cardiac hypertrophy and fibrosis: Serelaxin (SLX), a recombinant relaxin-2, decreases MiR-29 expression, activates Wnt- signaling and its components GSK3B, ICAT/CTNNBIP1, HBP1 and GLIS2, attenuates pathologic hypertrophy, inhibits fibrosis of the heart tissue, and improves cardiac function via upregulation of its target gene, 24/August/2018, 2.52 pm
Serelaxin (SLX)-based therapy for cardiac hypertrophy and fibrosis: Serelaxin (SLX), a recombinant relaxin-2, decreases MiR-29 expression, activates Wnt- signaling and its components GSK3B, ICAT/CTNNBIP1, HBP1 and GLIS2, attenuates pathologic hypertrophy, inhibits fibrosis of the heart tissue, and improves cardiac function via upregulation of its target gene, 24/August/2018, 2.52 pm 960 720 Dr Boomi's Genom-2-Discovery Center

Introduction: What they say: A recent study from the Institute of Pharmacology and Toxicology, Technical University Munich (TUM), 80802, Munich, Germany; DZHK (German Center for Cardiovascular Research), partner site Munich…

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Relax(in) your way to keep the cardiac diseases at bay: Relaxin-based Regenerative therapy for regaining the lost cardiomyocytes in Myocardial patients:  Relaxin, a reproductive hormone,  increases the expression of ERBB2/Her2 and promotes dedifferentiation  of cardiomyocytes via down-regulation of its target gene, 17/August/2018, 11.19 pm
Relax(in) your way to keep the cardiac diseases at bay: Relaxin-based Regenerative therapy for regaining the lost cardiomyocytes in Myocardial patients:  Relaxin, a reproductive hormone,  increases the expression of ERBB2/Her2 and promotes dedifferentiation  of cardiomyocytes via down-regulation of its target gene, 17/August/2018, 11.19 pm 960 720 Dr Boomi's Genom-2-Discovery Center

Introduction: What they say A recent study from the Department of Biological Regulation, Weizmann Institute of Science, Rehovot 76100, Israel shows that “ERBB2 triggers mammalian heart regeneration by promoting cardiomyocyte dedifferentiation and proliferation.” This study was published, in the 6 April…

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Flu vaccine preserves your heart function against cardiac diseases: Flu vaccine-based therapy for attenuating pathogenesis-associated with Myocardial infarction: Influenza A/flu(H1N1) vaccine decreases IRF3 (Interferon regulatory transcription factor-3), GM-CSF (Granulocyte-macrophage colony-stimulating factor) and GRK2(G protein-coupled receptor kinase) expression, inhibits undue leucocyte activation and invasion, suppresses recruitment of inflammatory cells, inhibits ventricular dilation, and promotes heart repair and survival, via up regulation of its target gene, 14/July/2018, 9.06 pm
Flu vaccine preserves your heart function against cardiac diseases: Flu vaccine-based therapy for attenuating pathogenesis-associated with Myocardial infarction: Influenza A/flu(H1N1) vaccine decreases IRF3 (Interferon regulatory transcription factor-3), GM-CSF (Granulocyte-macrophage colony-stimulating factor) and GRK2(G protein-coupled receptor kinase) expression, inhibits undue leucocyte activation and invasion, suppresses recruitment of inflammatory cells, inhibits ventricular dilation, and promotes heart repair and survival, via up regulation of its target gene, 14/July/2018, 9.06 pm 960 720 Dr Boomi's Genom-2-Discovery Center

Introduction: What they say: A recent study from Department of Systems Biology, Harvard Medical School, Boston, Massachusetts, USA; and Cardiovascular Research Center, Massachusetts General Hospital and Harvard Medical School, Boston,…

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