Ionized calcium (Ca2+) is the most versatile cellular messenger. All cells use Ca2+ signals to regulate their activities in response to extrinsic and intrinsic stimuli. Alterations in cellular Ca2+ signaling and/or Ca2+ homeostasis can subvert physiological processes into driving pathological outcomes. Imaging of living cells over the past decades has demonstrated that Ca2+ signals encode information in their frequency, kinetics, amplitude, and spatial extent. These parameters alter depending on the type and intensity of stimulation, and cellular context. Moreover, it is evident that different cell types produce widely varying Ca2+ signals, with properties that suit their physiological functions. This primer discusses basic principles and mechanisms underlying cellular Ca2+ signaling and Ca2+ homeostasis. Consequently, we have cited some historical articles in addition to more recent findings. A brief summary of the core features of cellular Ca2+ signaling is provided, with particular focus on Ca2+ stores and Ca2+ transport across cellular membranes, as well as mechanisms by which Ca2+ signals activate downstream effector systems.

/pdf/fundamentals-of-cellular-calcium-signaling-a-primer-1lcy03avxk.pdf

Fundamentals of Cellular Calcium Signaling: A Primer

Triboelectric nanogenerators (TENGs) have gained significant traction in recent years in the bioengineering community. With the potential for expansive applications for biomedical use, many individuals and research groups have furthered their studies on the topic, in order to gain an understanding of how TENGs can contribute to healthcare. More specifically, there have been a number of recent studies focusing on implantable triboelectric nanogenerators (I-TENGs) toward self-powered cardiac systems healthcare. In this review, the progression of implantable TENGs for self-powered cardiovascular healthcare, including self-powered cardiac monitoring devices, self-powered therapeutic devices, and power sources for cardiac pacemakers, will be systematically reviewed. Long-term expectations of these implantable TENG devices through their biocompatibility and other utilization strategies will also be discussed.

Implantable Triboelectric Nanogenerators for Self-Powered Cardiovascular Healthcare.

Effects of SGLT2 Inhibitors on Ion Homeostasis and Oxidative Stress associated Mechanisms in Heart Failure.

Cardiac pathology in neuronal ceroid lipofuscinoses (NCL): More than a mere co-morbidity

N-methyl-D-aspartate receptors (NMDARs) are ligand-gated ion channels that are activated by the neurotransmitter glutamate, mediate the slow component of excitatory neurotransmission in the central nervous system (CNS), and induce long-term changes in synaptic plasticity. NMDARs are non-selective cation channels that allow the influx of extracellular Na+ and Ca2+ and control cellular activity via both membrane depolarization and an increase in intracellular Ca2+ concentration. The distribution, structure, and role of neuronal NMDARs have been extensively investigated and it is now known that they also regulate crucial functions in the non-neuronal cellular component of the CNS, i.e., astrocytes and cerebrovascular endothelial cells. In addition, NMDARs are expressed in multiple peripheral organs, including heart and systemic and pulmonary circulations. Herein, we survey the most recent information available regarding the distribution and function of NMDARs within the cardiovascular system. We describe the involvement of NMDARs in the modulation of heart rate and cardiac rhythm, in the regulation of arterial blood pressure, in the regulation of cerebral blood flow, and in the blood–brain barrier (BBB) permeability. In parallel, we describe how enhanced NMDAR activity could promote ventricular arrhythmias, heart failure, pulmonary artery hypertension (PAH), and BBB dysfunction. Targeting NMDARs could represent an unexpected pharmacological strategy to reduce the growing burden of several life-threatening cardiovascular disorders.

/pdf/the-emerging-role-of-n-methyl-d-aspartate-nmda-receptors-in-1zgjsb8d.pdf

The Emerging Role of N-Methyl-D-Aspartate (NMDA) Receptors in the Cardiovascular System: Physiological Implications, Pathological Consequences, and Therapeutic Perspectives

Rhythmic increases in intracellular Ca2+ concentration underlie the contractile function of the heart. These heart muscle-wide changes in intracellular Ca2+ are induced and coordinated by electrical depolarization of the cardiomyocyte sarcolemma by the action potential. Originating at the sinoatrial node, conduction of this electrical signal throughout the heart ensures synchronization of individual myocytes into an effective cardiac pump. Ca2+ signaling pathways also regulate gene expression and cardiomyocyte growth during development and in pathology. These fundamental roles of Ca2+ in the heart are illustrated by the prevalence of altered Ca2+ homeostasis in cardiovascular diseases. Indeed, heart failure (an inability of the heart to support hemodynamic needs), rhythmic disturbances, and inappropriate cardiac growth all share an involvement of altered Ca2+ handling. The prevalence of these pathologies, contributing to a third of all deaths in the developed world as well as to substantial morbidity makes understanding the mechanisms of Ca2+ handling and dysregulation in cardiomyocytes of great importance.

/pdf/calcium-signaling-in-cardiomyocyte-function-2tpyurpvos.pdf

Calcium Signaling in Cardiomyocyte Function

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Calcium Signaling in Cardiomyocyte Function