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Cardiotoxicity of the BCR-ABL1 tyrosine kinase inhibitors: Emphasis on ponatinib

International journal of cardiology, 2020-10, Vol.316, p.214-221

2020

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Inhibition of GSK-3 to induce cardiomyocyte proliferation: a recipe for in situ cardiac regeneration

Cardiovascular research, 2019-01, Vol.115 (1), p.20-30

2019

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Mechanisms of Fibroblast Activation and Myocardial Fibrosis: Lessons Learned from FB-Specific Conditional Mouse Models

Cells (Basel, Switzerland), 2021-09, Vol.10 (9), p.2412

2021

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Mitochondrial Peroxiredoxin-3 protects against hyperglycemia induced myocardial damage in Diabetic cardiomyopathy

Free radical biology & medicine, 2016-08, Vol.97, p.489-500

2016

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Monoamine oxidase-A is an important source of oxidative stress and promotes cardiac dysfunction, apoptosis, and fibrosis in diabetic cardiomyopathy

Free radical biology & medicine, 2015-10, Vol.87, p.263-273

2015

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Cardiomyocyte SMAD4-Dependent TGF-β Signaling is Essential to Maintain Adult Heart Homeostasis

JACC. Basic to translational science, 2019-02, Vol.4 (1), p.41-53

2019

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Isoform-Specific Role of GSK-3 in High Fat Diet Induced Obesity and Glucose Intolerance

Cells (Basel, Switzerland), 2022-02, Vol.11 (3), p.559

2022

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Sustained Increases in Cardiomyocyte Protein O -Linked β-N-Acetylglucosamine Levels Lead to Cardiac Hypertrophy and Reduced Mitochondrial Function Without Systolic Contractile Impairment

Journal of the American Heart Association, 2023-10, Vol.12 (19), p.e029898

2023

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Deletion of Cardiomyocyte Glycogen Synthase Kinase-3 Beta (GSK-3β) Improves Systemic Glucose Tolerance with Maintained Heart Function in Established Obesity

Cells (Basel, Switzerland), 2020-04, Vol.9 (5), p.1120

2020

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The BDNF rs6265 Polymorphism is a Modifier of Cardiomyocyte Contractility and Dilated Cardiomyopathy

International journal of molecular sciences, 2020-10, Vol.21 (20), p.7466

2020

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Animal Models of Haploinsufficiency Revealed the Isoform-Specific Role of GSK-3 in HFD-Induced Obesity and Glucose Intolerance

American Journal of Physiology: Cell Physiology, 2024-09

2024

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Entanglement of GSK-3β, β-catenin and TGF-β1 signaling network to regulate myocardial fibrosis

Journal of molecular and cellular cardiology, 2017-09, Vol.110, p.109-120

2017

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Fibroblast GSK-3α Promotes Fibrosis via RAF-MEK-ERK Pathway in the Injured Heart

Circulation research, 2022-09, Vol.131 (7), p.620-636

2022

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Abstract P3056: Cardiac Fibroblast GSK-3α Contributes To Chronic Inflammation In The Ischemic Heart

Circulation research, 2023-08, Vol.133 (Suppl_1)

2023

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Repurposing Nintedanib for pathological cardiac remodeling and dysfunction

Pharmacological research, 2021-07, Vol.169, p.105605-105605, Article 105605

2021

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Abstract EC106: Cardiac Fibroblast GSK-3α Aggravates Ischemic Cardiac Injury By Promoting Fibrosis, Inflammation, And Impairing Angiogenesis

Circulation research, 2022-08, Vol.131 (Suppl_1)

2022

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Abstract 530: Cardiac Fibroblast GSK-3α Contributes to Ventricular Remodeling and Dysfunction of the Failing Heart

Circulation research, 2019-08, Vol.125 (Suppl_1)

2019

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Abstract P3065: Mechanistic Insights Into Cardiac Dysfunction And Remodeling Associated With Invasive Pneumococcal Pathogenesis

Circulation research, 2023-08, Vol.133 (Suppl_1)

2023

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Abstract P2005: Mechanosensitive Piezo-1 Channel Aggravates Ischemia Induced Adverse Cardiac Remodeling And Dysfunction

Circulation research, 2023-08, Vol.133 (Suppl_1)

2023

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Ponatinib-induced cardiotoxicity: delineating the signalling mechanisms and potential rescue strategies

Cardiovascular research, 2019-04, Vol.115 (5), p.966-977

2019

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Abstract P317: Cardiac Fibroblast GSK3α Promotes Myocardial Fibrotic Remodeling Through GSK3α-ERK-IL11 Signaling Circuit

Circulation research, 2021-09, Vol.129 (Suppl_1)

2021

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Abstract We061: Cardiomyocytes HIPK2 Regulates Myocardial Inflammation And Heart Function Through Purinergic Signaling

Circulation research, 2024-08, Vol.135 (Suppl_1)

2024

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Ponatinib Drives Cardiotoxicity by S100A8/A9-NLRP3-IL-1β Mediated Inflammation

Circulation research, 2023-02, Vol.132 (3), p.267-289

2023

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Abstract GS109: Ponatinib-induced Cardiotoxicity Is Driven By S100A8/A9-NLRP3-IL1β Signaling Mediated Excessive Inflammation

Circulation research, 2022-08, Vol.131 (Suppl_1)

2022

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GSK-3 at the heart of cardiometabolic diseases: Isoform-specific targeting is critical to therapeutic benefit

Biochimica et biophysica acta. Molecular basis of disease, 2023-08, Vol.1869 (6), p.166724-166724, Article 166724

2023

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Cardiotoxicity of the BCR-ABL1 tyrosine kinase inhibitors: Emphasis on ponatinib

Inhibition of GSK-3 to induce cardiomyocyte proliferation: a recipe for in situ cardiac regeneration

Mechanisms of Fibroblast Activation and Myocardial Fibrosis: Lessons Learned from FB-Specific Conditional Mouse Models

Mitochondrial Peroxiredoxin-3 protects against hyperglycemia induced myocardial damage in Diabetic cardiomyopathy

Monoamine oxidase-A is an important source of oxidative stress and promotes cardiac dysfunction, apoptosis, and fibrosis in diabetic cardiomyopathy

Cardiomyocyte SMAD4-Dependent TGF-β Signaling is Essential to Maintain Adult Heart Homeostasis

Isoform-Specific Role of GSK-3 in High Fat Diet Induced Obesity and Glucose Intolerance

Sustained Increases in Cardiomyocyte Protein O -Linked β-N-Acetylglucosamine Levels Lead to Cardiac Hypertrophy and Reduced Mitochondrial Function Without Systolic Contractile Impairment

Deletion of Cardiomyocyte Glycogen Synthase Kinase-3 Beta (GSK-3β) Improves Systemic Glucose Tolerance with Maintained Heart Function in Established Obesity

The BDNF rs6265 Polymorphism is a Modifier of Cardiomyocyte Contractility and Dilated Cardiomyopathy

Animal Models of Haploinsufficiency Revealed the Isoform-Specific Role of GSK-3 in HFD-Induced Obesity and Glucose Intolerance

Entanglement of GSK-3β, β-catenin and TGF-β1 signaling network to regulate myocardial fibrosis

Fibroblast GSK-3α Promotes Fibrosis via RAF-MEK-ERK Pathway in the Injured Heart

Abstract P3056: Cardiac Fibroblast GSK-3α Contributes To Chronic Inflammation In The Ischemic Heart

Repurposing Nintedanib for pathological cardiac remodeling and dysfunction

Abstract EC106: Cardiac Fibroblast GSK-3α Aggravates Ischemic Cardiac Injury By Promoting Fibrosis, Inflammation, And Impairing Angiogenesis

Abstract 530: Cardiac Fibroblast GSK-3α Contributes to Ventricular Remodeling and Dysfunction of the Failing Heart

Abstract P3065: Mechanistic Insights Into Cardiac Dysfunction And Remodeling Associated With Invasive Pneumococcal Pathogenesis

Abstract P2005: Mechanosensitive Piezo-1 Channel Aggravates Ischemia Induced Adverse Cardiac Remodeling And Dysfunction

Ponatinib-induced cardiotoxicity: delineating the signalling mechanisms and potential rescue strategies

Abstract P317: Cardiac Fibroblast GSK3α Promotes Myocardial Fibrotic Remodeling Through GSK3α-ERK-IL11 Signaling Circuit

Abstract We061: Cardiomyocytes HIPK2 Regulates Myocardial Inflammation And Heart Function Through Purinergic Signaling

Ponatinib Drives Cardiotoxicity by S100A8/A9-NLRP3-IL-1β Mediated Inflammation

Abstract GS109: Ponatinib-induced Cardiotoxicity Is Driven By S100A8/A9-NLRP3-IL1β Signaling Mediated Excessive Inflammation

GSK-3 at the heart of cardiometabolic diseases: Isoform-specific targeting is critical to therapeutic benefit

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