Under normal, healthy conditions, the contraction of cardiac myocytes, leading to the pump function of this organ, is driven by calcium-dependent mechanisms. Entry of calcium into the myocyte during the cardiac action potential causes activation of the ryanodine receptors and release of calcium from the sarcoplasmic reticulum (SR). This process of calcium-induced calcium release is essential for excitation-contraction coupling and enables each action potential to be transduced into a mechanical event. Indeed, in healthy myocytes, the calcium concentration in the cytosol of is elevated approximately 10-fold from a resting level of ~100 nM to ~1 µM. This process is finely orchestrated by a number of key proteins, which can be specifically regulated by various pathways depending on the oxygen demand. Furthermore, the specific structure of the myocyte allows certain calcium-dependent processes to be compartmentalised, increasing the efficiency of this regulation.
Heart failure is a common, costly, and life-threatening condition. In 2015, for example, it affected around 40 million people globally. In patients with heart failure, the risk of sudden cardiac death and arrhythmias increases substantially. Cellular remodelling and alterations in calcium handling, which appear to contribute to this increase in arrhythmogenicity, have been extensively reported. However, there remains a number of unanswered questions, and each new study on this subject raises additional novel questions. Further research is, therefore, required regarding the link between calcium, heart failure and any associated arrhythmias to allow us to fully comprehend, and ultimately utilise these connections.
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 which will give further insights into the role of calcium handling during heart failure. 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, that may lead to therapeutic options for the future.
Under normal, healthy conditions, the contraction of cardiac myocytes, leading to the pump function of this organ, is driven by calcium-dependent mechanisms. Entry of calcium into the myocyte during the cardiac action potential causes activation of the ryanodine receptors and release of calcium from the sarcoplasmic reticulum (SR). This process of calcium-induced calcium release is essential for excitation-contraction coupling and enables each action potential to be transduced into a mechanical event. Indeed, in healthy myocytes, the calcium concentration in the cytosol of is elevated approximately 10-fold from a resting level of ~100 nM to ~1 µM. This process is finely orchestrated by a number of key proteins, which can be specifically regulated by various pathways depending on the oxygen demand. Furthermore, the specific structure of the myocyte allows certain calcium-dependent processes to be compartmentalised, increasing the efficiency of this regulation.
Heart failure is a common, costly, and life-threatening condition. In 2015, for example, it affected around 40 million people globally. In patients with heart failure, the risk of sudden cardiac death and arrhythmias increases substantially. Cellular remodelling and alterations in calcium handling, which appear to contribute to this increase in arrhythmogenicity, have been extensively reported. However, there remains a number of unanswered questions, and each new study on this subject raises additional novel questions. Further research is, therefore, required regarding the link between calcium, heart failure and any associated arrhythmias to allow us to fully comprehend, and ultimately utilise these connections.
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 which will give further insights into the role of calcium handling during heart failure. 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, that may lead to therapeutic options for the future.
