Cardiac Protein Kinases as Homeostatic Molecular “Switches” and Regulators of Cell Fate

Dear Colleagues,

A plethora of biological processes are regulated by protein kinases, which constitute one of the major supergene families. As effectors of signal transduction, protein kinase pathways integrate exogenous signals and orchestrate multiple aspects of cell function, including growth, differentiation, proliferation, metabolism, gene expression, survival, and apoptosis. Thus, they act as determinants of cell fate, balancing survival or death, under both physiological and pathological conditions. Given the increasing prevalence and morbidity of cardiovascular diseases, studying the role of kinases in myocardial function is of critical significance. Molecular, translational, and clinical studies could shed light on the complex mechanisms regulating interplay and crosstalk of cardiac protein kinase pathways. The latter exert redundant functions via phosphorylation of substrates as diverse as cytoskeletal proteins, cell cycle or apoptotic regulators and transcription factors, thereby eliciting a wide range of responses. Activated in a spatiotemporal manner, kinase signaling pathways are involved in the preservation of cardiac homeostasis by regulating cardiac compensatory hypertrophy, excitation–contraction coupling, metabolism, energetics or autophagy. On the other hand, when activated under stress conditions (i.e., by oxidative insults or osmotic imbalances), they may also confer detrimental effects by compromising optimal cell function and favoring cell death. Consequently, they contribute to the progression of several pathologies, including maladaptive eccentric hypertrophy, ischemia reperfusion injury, myocardial infarction, hypertension, arrhythmias, cardiomyopathies, and heart failure. Intensity, duration, and subcellular localization of kinase signaling determine the end-response. Thus, understanding and delineating cardiac protein kinase mechanisms of action may contribute to elucidation of their central role in cardiac physiology and in novel therapeutic approaches for cardiovascular diseases.

Dr. Ioanna-Katerina Aggeli
Guest Editor

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• signal transduction
• protein kinases
• cardiovascular diseases
• stress
• gene expression
• survival
• cell death
• autophagy