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Dual inhibition of cathepsin G and chymase reduces myocyte death and improves cardiac remodeling after myocardial ischemia reperfusion injury

Basic research in cardiology, 2017-11, Vol.112 (6), p.62-13, Article 62

2017

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c-Cbl Inhibition Improves Cardiac Function and Survival in Response to Myocardial Ischemia

Circulation (New York, N.Y.), 2014-05, Vol.129 (20), p.2031-2043

2014

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Inflammatory Serine Proteases Play a Critical Role in the Early Pathogenesis of Diabetic Cardiomyopathy

Cellular physiology and biochemistry, 2019, Vol.53 (6), p.982-998

2019

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c-Cbl Ubiquitin Ligase Regulates Focal Adhesion Protein Turnover and Myofibril Degeneration Induced by Neutrophil Protease Cathepsin G

The Journal of biological chemistry, 2012-02, Vol.287 (8), p.5327-5339

2012

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Cardiac Expression of Factor X Mediates Cardiac Hypertrophy and Fibrosis in Pressure Overload

JACC. Basic to translational science, 2020-01, Vol.5 (1), p.69-83

2020

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RETRACTED: Cardiac Expression of Factor X Mediates Cardiac Hypertrophy and Fibrosis in Pressure Overload

JACC. Basic to translational science, 2020-01, Vol.5 (1), p.69-83

2020

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Abstract 3137: The Role Of Rna Binding Protein Fxr1 In Regulating Methylated Mrna Transcript Stability And Vascular Smooth Muscle Cell Contractility

Arteriosclerosis, thrombosis, and vascular biology, 2024-05, Vol.44 (Suppl_1)

2024

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Culture of primary rat hepatocytes within porous chitosan scaffolds

Journal of biomedical materials research, 2003-12, Vol.67A (3), p.938-943

2003

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GDF11 Does Not Rescue Aging-Related Pathological Hypertrophy

Circulation research, 2015-11, Vol.117 (11), p.926-932

2015

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Abstract 15113: C-cbl E3 Ubiquitin Ligase Regulates Cardiomyocyte Proliferation and Cardiac Regeneration

Circulation (New York, N.Y.), 2022-11, Vol.146 (Suppl_1)

2022

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Interaction study of LDL with charged ligands for effective LDL-C-removing adsorbents

Reactive & functional polymers, 2008, Vol.68 (1), p.261-267

2008

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Loss of Protease-Activated Receptor 4 Prevents Inflammation Resolution and Predisposes the Heart to Cardiac Rupture After Myocardial Infarction

Circulation (New York, N.Y.), 2020-08, Vol.142 (8), p.758-775

2020

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Intracardiac administration of neutrophil protease cathepsin G activates noncanonical inflammasome pathway and promotes inflammation and pathological remodeling in non-injured heart

Journal of molecular and cellular cardiology, 2019-09, Vol.134, p.29-39

2019

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Protease-activated receptor 4 deficiency offers cardioprotection after acute ischemia reperfusion injury

Journal of molecular and cellular cardiology, 2016-01, Vol.90, p.21-29

2016

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Differential microRNA-21 and microRNA-221 Upregulation in the Biventricular Failing Heart Reveals Distinct Stress Responses of Right Versus Left Ventricular Fibroblasts

Circulation. Heart failure, 2020-01, Vol.13 (1), p.e006426-e006426

2020

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Inhibition of inflammatory serine proteases promotes vascularization and enhances cardiac repair after myocardial infarction

Journal of molecular and cellular cardiology, 2018-11, Vol.124, p.92-93

2018

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Targeting inflammatory serine proteases for cardiac repair after Ischemia Reperfusion injury (1080.10)

The FASEB journal, 2014-04, Vol.28 (S1), p.n/a

2014

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DPPI Deficiency Enhances Both Angiogenesis and Arteriogenesis and Improves Cardiac Function after Myocardial Infarction

The FASEB journal, 2016-04, Vol.30 (S1)

2016

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Cardiac Expression of Factor X Mediates Cardiac Hypertrophy and Fibrosis in Pressure Overload

JACC. Basic to translational science, 2022-09, Vol.7 (9), p.970-971

2022

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Death‐associated protein kinase mediates myofibril degeneration and myocyte apoptosis induced by beta‐adrenergic receptors (404.3)

The FASEB journal, 2014-04, Vol.28 (S1), p.n/a

2014

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Beta1-adrenergic receptors promote focal adhesion signaling downregulation and myocyte apoptosis in acute volume overload

Journal of molecular and cellular cardiology, 2012-08, Vol.53 (2), p.240-249

2012

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Abstract 126: Gene Deletion of Dipeptidyl Peptidase I Reduces Myocyte Loss and Preserves Cardiac Function After Myocardial Ischemia-Reperfusion Injury

Circulation research, 2012-08, Vol.111 (suppl_1)

2012

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Abstract 214: Cbl Inhibition Improves Cardiac Function and Survival in Response to Myocardial Ischemia

Circulation research, 2012-08, Vol.111 (suppl_1)

2012

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Enhanced, simplified expression of perdeuterated hemoglobin for NMR structure and dynamics

Protein expression and purification, 2010-07, Vol.72 (1), p.8-18

2010

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Abstract 15876: Cbl E3 Ubiquitin Ligase Activation Promotes Myocyte Death and Leads to Pathological Cardiac Hypertrophy After Pressure Overload

Circulation (New York, N.Y.), 2018-11, Vol.138 (Suppl_1 Suppl 1), p.A15876-A15876

2018

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Dual inhibition of cathepsin G and chymase reduces myocyte death and improves cardiac remodeling after myocardial ischemia reperfusion injury

c-Cbl Inhibition Improves Cardiac Function and Survival in Response to Myocardial Ischemia

Inflammatory Serine Proteases Play a Critical Role in the Early Pathogenesis of Diabetic Cardiomyopathy

c-Cbl Ubiquitin Ligase Regulates Focal Adhesion Protein Turnover and Myofibril Degeneration Induced by Neutrophil Protease Cathepsin G

Cardiac Expression of Factor X Mediates Cardiac Hypertrophy and Fibrosis in Pressure Overload

RETRACTED: Cardiac Expression of Factor X Mediates Cardiac Hypertrophy and Fibrosis in Pressure Overload

Abstract 3137: The Role Of Rna Binding Protein Fxr1 In Regulating Methylated Mrna Transcript Stability And Vascular Smooth Muscle Cell Contractility

Culture of primary rat hepatocytes within porous chitosan scaffolds

GDF11 Does Not Rescue Aging-Related Pathological Hypertrophy

Abstract 15113: C-cbl E3 Ubiquitin Ligase Regulates Cardiomyocyte Proliferation and Cardiac Regeneration

Interaction study of LDL with charged ligands for effective LDL-C-removing adsorbents

Loss of Protease-Activated Receptor 4 Prevents Inflammation Resolution and Predisposes the Heart to Cardiac Rupture After Myocardial Infarction

Intracardiac administration of neutrophil protease cathepsin G activates noncanonical inflammasome pathway and promotes inflammation and pathological remodeling in non-injured heart

Protease-activated receptor 4 deficiency offers cardioprotection after acute ischemia reperfusion injury

Differential microRNA-21 and microRNA-221 Upregulation in the Biventricular Failing Heart Reveals Distinct Stress Responses of Right Versus Left Ventricular Fibroblasts

Inhibition of inflammatory serine proteases promotes vascularization and enhances cardiac repair after myocardial infarction

Targeting inflammatory serine proteases for cardiac repair after Ischemia Reperfusion injury (1080.10)

DPPI Deficiency Enhances Both Angiogenesis and Arteriogenesis and Improves Cardiac Function after Myocardial Infarction

Cardiac Expression of Factor X Mediates Cardiac Hypertrophy and Fibrosis in Pressure Overload

Death‐associated protein kinase mediates myofibril degeneration and myocyte apoptosis induced by beta‐adrenergic receptors (404.3)

Beta1-adrenergic receptors promote focal adhesion signaling downregulation and myocyte apoptosis in acute volume overload

Abstract 126: Gene Deletion of Dipeptidyl Peptidase I Reduces Myocyte Loss and Preserves Cardiac Function After Myocardial Ischemia-Reperfusion Injury

Abstract 214: Cbl Inhibition Improves Cardiac Function and Survival in Response to Myocardial Ischemia

Enhanced, simplified expression of perdeuterated hemoglobin for NMR structure and dynamics

Abstract 15876: Cbl E3 Ubiquitin Ligase Activation Promotes Myocyte Death and Leads to Pathological Cardiac Hypertrophy After Pressure Overload

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