Ali El-Armouche

Linking superinhibitory PLN mutations to CaMKII activation: a new arrhythmogenic mechanism in genetic DCM?

Adipocyte-Specific Hypoxia-Inducible Factor 2α Deficiency Exacerbates Obesity-Induced Brown Adipose Tissue Dysfunction and Metabolic Dysregulation.

Phosphodiesterase 2: anti-adrenergic friend or hypertrophic foe in heart disease?

Role of protein phosphatase inhibitor-1 in cardiac beta adrenergic pathway.

Phosphodiesterase 2 Protects Against Catecholamine-Induced Arrhythmia and Preserves Contractile Function After Myocardial Infarction.

Comment on Ferrannini et al. CV Protection in the EMPA-REG OUTCOME Trial: A "Thrifty Substrate" Hypothesis. Diabetes Care 2016;39:1108-1114.

Sex-difference in expression and function of beta-adrenoceptors in macrovessels: role of the endothelium.

Chronic loss of inhibitor-1 diminishes cardiac RyR2 phosphorylation despite exaggerated CaMKII activity.

Calcium/Calmodulin-Dependent Protein Kinase II Activity Persists During Chronic β-Adrenoceptor Blockade in Experimental and Human Heart Failure.

Differential regulation of protein phosphatase 1 (PP1) isoforms in human heart failure and atrial fibrillation.

PDE2 at the crossway between cAMP and cGMP signalling in the heart.

Erratum to: Differential regulation of protein phosphatase 1 (PP1) isoforms in human heart failure and atrial fibrillation.

A proteolytic fragment of histone deacetylase 4 protects the heart from failure by regulating the hexosamine biosynthetic pathway.

Ectopic expression of S28A-mutated Histone H3 modulates longevity, stress resistance and cardiac function in Drosophila.

MicroRNAs in cardiomyocyte differentiation and maturation.

Hematopoietic hypoxia-inducible factor 2α deficiency ameliorates pathological retinal neovascularization via modulation of endothelial cell apoptosis.

Activation of protein phosphatase 1 by a selective phosphatase disrupting peptide reduces sarcoplasmic reticulum Ca leak in human heart failure.

The reduced activity of PP-1α under redox stress condition is a consequence of GSH-mediated transient disulfide formation.

Protein kinase/phosphatase balance mediates the effects of increased late sodium current on ventricular calcium cycling.

Estrogen determines sex differences in adrenergic vessel tone by regulation of endothelial β-adrenoceptor expression.