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

A special issue of Biology (ISSN 2079-7737). This special issue belongs to the section "Medical Biology".

Deadline for manuscript submissions: 31 January 2022.

Special Issue Editor

Dr. Ioanna-Katerina Aggeli
E-Mail Website
Guest Editor
Department of Animal and Human Physiology, School of Biology, University of Athens, University Campus, 157 84 Athens, Greece
Interests: signal transduction pathways; protein kinases; heart; cardiac myocytes; oxidative stress; apoptosis; autophagy; stress sensors

Special Issue Information

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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Keywords

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

Published Papers (2 papers)

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Research

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Article
PI3K as Mediator of Apoptosis and Contractile Dysfunction in TGFβ1-Stimulated Cardiomyocytes
Biology 2021, 10(7), 670; https://doi.org/10.3390/biology10070670 - 16 Jul 2021
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Abstract
Background: TGFβ1 is a growth factor that plays a major role in the remodeling process of the heart by inducing cardiomyocyte dysfunction and apoptosis, as well as fibrosis thereby restricting heart function. TGFβ1 mediates its effect via the TGFβ receptor I [...] Read more.
Background: TGFβ1 is a growth factor that plays a major role in the remodeling process of the heart by inducing cardiomyocyte dysfunction and apoptosis, as well as fibrosis thereby restricting heart function. TGFβ1 mediates its effect via the TGFβ receptor I (ALK5) and the activation of SMAD transcription factors, but TGFβ1 is also known as activator of phosphoinositide-3-kinase (PI3K) via the non-SMAD signaling pathway. The aim of this study was to investigate whether PI3K is also involved in TGFβ1–induced cardiomyocytes apoptosis and contractile dysfunction. Methods and Results: Incubation of isolated ventricular cardiomyocytes with TGFβ1 resulted in impaired contractile function. Pre-incubation of cells with the PI3K inhibitor Ly294002 or the ALK5 inhibitor SB431542 attenuated the decreased cell shortening in TGFβ1–stimulated cells. Additionally, TGFβ-induced apoptosis was significantly reduced by the PI3K inhibitor Ly294002. Administration of a PI3Kγ-specific inhibitor AS605240 abolished the TGFβ effect on apoptosis and cell shortening. This was also confirmed in cardiomyocytes from PI3Kγ KO mice. Induction of SMAD binding activity and the TGFβ target gene collagen 1 could be blocked by the PI3K inhibitor Ly294002, but not by the specific PI3Kγ inhibitor AS605240. Conclusions: TGFβ1-induced SMAD activation, cardiomyocyte apoptosis, and impaired cell shortening are mediated via both, the ALK5 receptor and PI3K, in adult cardiomyocytes. PI3Kγ specifically contributes to apoptosis induction and impairment of contractile function independent of SMAD signaling. Full article
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Review

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Review
ERK1/2: An Integrator of Signals That Alters Cardiac Homeostasis and Growth
Biology 2021, 10(4), 346; https://doi.org/10.3390/biology10040346 - 20 Apr 2021
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Abstract
Integration of cellular responses to extracellular cues is essential for cell survival and adaptation to stress. Extracellular signal-regulated kinase (ERK) 1 and 2 serve an evolutionarily conserved role for intracellular signal transduction that proved critical for cardiomyocyte homeostasis and cardiac stress responses. Considering [...] Read more.
Integration of cellular responses to extracellular cues is essential for cell survival and adaptation to stress. Extracellular signal-regulated kinase (ERK) 1 and 2 serve an evolutionarily conserved role for intracellular signal transduction that proved critical for cardiomyocyte homeostasis and cardiac stress responses. Considering the importance of ERK1/2 in the heart, understanding how these kinases operate in both normal and disease states is critical. Here, we review the complexity of upstream and downstream signals that govern ERK1/2-dependent regulation of cardiac structure and function. Particular emphasis is given to cardiomyocyte hypertrophy as an outcome of ERK1/2 activation regulation in the heart. Full article
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