About this Research Topic
This Research Topic is part of the Calcium and Heart Failure series: Volume I
Heart Failure (HF) has been previously described as the cardiovascular epidemic of the 21st century, and although there has been progress in developing novel treatments of HF, for example SGLT2 inhibitors, there remains an unmet clinical need to increase our pharmacological arsenal against HF.
In patients with HF, the risk of sudden cardiac death and arrhythmias increases substantially. Calcium plays a critical role in the link of electrical excitation and contractile function of myocytes as well as controlling other calcium-dependent mechanisms, such as heart rate, and more intricate balances of gene expression.
Cellular remodeling and alterations in calcium handling during HF, appear to contribute to the HF phenotype, which includes the increase in arrhythmogenicity. A number of these alterations have previously been extensively reported, especially in HF with reduced ejection fraction (HFrEF), although the complete picture remains elusive, with new questions being continually posed to fully understand the contribution calcium handling plays in HF pathology. Furthermore, studies regarding calcium handling in HF with preserved ejection fraction (HPpEF) remain limited. Further research is, therefore, required regarding the link between calcium, HF and any associated arrhythmias to allow us to fully comprehend, and ultimately utilise these connections to specifically target calcium handling proteins as potential therapeutic agents.
For these reasons, we welcome experts on this research topic to share their original research, ranging from studies at the molecular level up to the whole organism and into the clinic which will give further insights into the role of calcium handling during HF, and how we can harness these mechanisms to develop novel therapeutics. In addition, given recent developments in novel technologies such as optogenetics and tissue engineering, we also encourage authors from this field to share their work on how these techniques can be applied to research of excitation/contraction coupling and HF.
Furthermore, solid review papers discussing the role of calcium in the pathophysiology of heart failure, as well as its undeniable role in arrhythmogenesis, would be most welcome. This compendium of articles will, therefore, be composed of state of the art overviews of this topic as well as provide novel insights, giving us an overview of the role of calcium in HF, ranging from the bench to the bedside.
Heart Failure (HF) has been previously described as the cardiovascular epidemic of the 21st century, and although there has been progress in developing novel treatments of HF, for example SGLT2 inhibitors, there remains an unmet clinical need to increase our pharmacological arsenal against HF.
In patients with HF, the risk of sudden cardiac death and arrhythmias increases substantially. Calcium plays a critical role in the link of electrical excitation and contractile function of myocytes as well as controlling other calcium-dependent mechanisms, such as heart rate, and more intricate balances of gene expression.
Cellular remodeling and alterations in calcium handling during HF, appear to contribute to the HF phenotype, which includes the increase in arrhythmogenicity. A number of these alterations have previously been extensively reported, especially in HF with reduced ejection fraction (HFrEF), although the complete picture remains elusive, with new questions being continually posed to fully understand the contribution calcium handling plays in HF pathology. Furthermore, studies regarding calcium handling in HF with preserved ejection fraction (HPpEF) remain limited. Further research is, therefore, required regarding the link between calcium, HF and any associated arrhythmias to allow us to fully comprehend, and ultimately utilise these connections to specifically target calcium handling proteins as potential therapeutic agents.
For these reasons, we welcome experts on this research topic to share their original research, ranging from studies at the molecular level up to the whole organism and into the clinic which will give further insights into the role of calcium handling during HF, and how we can harness these mechanisms to develop novel therapeutics. In addition, given recent developments in novel technologies such as optogenetics and tissue engineering, we also encourage authors from this field to share their work on how these techniques can be applied to research of excitation/contraction coupling and HF.
Furthermore, solid review papers discussing the role of calcium in the pathophysiology of heart failure, as well as its undeniable role in arrhythmogenesis, would be most welcome. This compendium of articles will, therefore, be composed of state of the art overviews of this topic as well as provide novel insights, giving us an overview of the role of calcium in HF, ranging from the bench to the bedside.
Keywords: Calcium, Arrhythmia, Heart Failure, Electrophysiology, EC Coupling, Pharmacology
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