Julie R. McMullen

Protective effects of exercise and phosphoinositide 3-kinase(p110alpha) signaling in dilated and hypertrophic cardiomyopathy.

Differences between pathological and physiological cardiac hypertrophy: novel therapeutic strategies to treat heart failure.

PI3K(p110alpha) inhibitors as anti-cancer agents: minding the heart.

Role of insulin-like growth factor 1 and phosphoinositide 3-kinase in a setting of heart disease.

β-Adrenergic Stimulation Induces Histone Deacetylase 5 (HDAC5) Nuclear Accumulation in Cardiomyocytes by B55α-PP2A-Mediated Dephosphorylation.

Phosphoinositide 3-kinase (p110α) gene delivery limits diabetes-induced cardiac NADPH oxidase and cardiomyopathy in a mouse model with established diastolic dysfunction.

The Interplay of Protein Coding and Non-Coding RNAs (circRNAs, lncRNAs) During Cardiac Differentiation.

The IGF1-PI3K-Akt Signaling Pathway in Mediating Exercise-Induced Cardiac Hypertrophy and Protection.

Distinct lipidomic profiles in models of physiological and pathological cardiac remodeling, and potential therapeutic strategies.

Understanding Key Mechanisms of Exercise-Induced Cardiac Protection to Mitigate Disease: Current Knowledge and Emerging Concepts.

Gene delivery of medium chain acyl-coenzyme A dehydrogenase induces physiological cardiac hypertrophy and protects against pathological remodelling.

Upregulated galectin-3 is not a critical disease mediator of cardiomyopathy induced by β-adrenoceptor overexpression.

Standing up to the cardiometabolic consequences of hematological cancers.

Divergent Effects of PKC (Protein Kinase C) α in the Human and Animal Heart? Therapeutic Implications for PKC Inhibitors in Cardiac Patients.

Improving the quality of preclinical research echocardiography: observations, training, and guidelines for measurement.

Adeno-Associated Virus Gene Therapy: Translational Progress and Future Prospects in the Treatment of Heart Failure.

Mechanisms responsible for increased circulating levels of galectin-3 in cardiomyopathy and heart failure.

PP2A negatively regulates the hypertrophic response by dephosphorylating HDAC2 S394 in the heart.

Lipidomic Profiles of the Heart and Circulation in Response to Exercise versus Cardiac Pathology: A Resource of Potential Biomarkers and Drug Targets.

Generation of MicroRNA-34 Sponges and Tough Decoys for the Heart: Developments and Challenges.

Galectin-3 deficiency ameliorates fibrosis and remodeling in dilated cardiomyopathy mice with enhanced Mst1 signaling.

Multiple receptors converge on H2-Q10 to regulate NK and γδT-cell development.

Noncoding RNAs regulating cardiac muscle mass.

Inhibition of heat shock protein 70 blocks the development of cardiac hypertrophy by modulating the phosphorylation of histone deacetylase 2.

Author Correction: PP2A negatively regulates the hypertrophic response by dephosphorylating HDAC2 S394 in the heart.

CORP: Practical tools for improving experimental design and reporting of laboratory studies of cardiovascular physiology and metabolism.

Gene therapy targeting cardiac phosphoinositide 3-kinase (p110α) attenuates cardiac remodeling in type 2 diabetes.

Clusterin is regulated by IGF1-PI3K signaling in the heart: implications for biomarker and drug target discovery, and cardiotoxicity.

Andersen-Tawil Syndrome Is Associated With Impaired PIP Regulation of the Potassium Channel Kir2.1.

Novel Lipid Species for Detecting and Predicting Atrial Fibrillation in Patients With Type 2 Diabetes.

IGF1-PI3K-induced physiological cardiac hypertrophy: Implications for new heart failure therapies, biomarkers, and predicting cardiotoxicity.

Correction for McMullen et al., "Deletion of Ribosomal S6 Kinases Does Not Attenuate Pathological, Physiological, or Insulin-Like Growth Factor 1 Receptor-Phosphoinositide 3-Kinase-Induced Cardiac Hypertrophy".

FoxO1 is required for physiological cardiac hypertrophy induced by exercise but not by constitutively active PI3K.

Old Drug, New Trick: Tilorone, a Broad-Spectrum Antiviral Drug as a Potential Anti-Fibrotic Therapeutic for the Diseased Heart.

Proteome characterisation of extracellular vesicles isolated from heart.

Prevention of Pathological Atrial Remodeling and Atrial Fibrillation: JACC State-of-the-Art Review.

A protocol for rapid and parallel isolation of myocytes and non-myocytes from multiple mouse hearts.

Overexpression of Heat Shock Protein 70 Improves Cardiac Remodeling and Survival in Protein Phosphatase 2A-Expressing Transgenic Mice with Chronic Heart Failure.