Changes in the numbers, phenotypes and electrophysiological properties of leukocytes frequently gave rise to arrhythmias, such as atrial fibrillation and ventricular arrhythmia, in patients with myocardial ischemia/infarction, heart failure and myocarditis. Many underlying conditions are associated with the inflammatory component and arrhythmia. For example, macrophages electrotonically couple to cardiomyocytes via connexin 43-containing gap junctions; immune cells interact with neural systems that influence information transfer; cytokines impact ion channel expression and function. These clinical associations between inflammatory indicators and arrhythmia incidence provide molecular insights. mmunotherapy is emerging as a potential treatment option for rhythm disorders, although more exploration is needed in the future. In this topic, we aim to bridge the knowledge gap between electrophysiology and immunology, promote conceptual connections between these two fields and explore promising opportunities for future clinical arrhythmia prevention and therapy.
We aim to discover innovative basic mechanism for clinical cardiac arrhythmias, and explore novel immunotherapy or immunomodulation strategies that can directly resolve immune-related arrhythmias. It is noteworthy that functional mechanism of monocytes, macrophages, natural killer cells, T cells, and other engineered immune cells on electrophysiology character such as autonomic nerve regulation and ion channel regulation are of particularly interest in this research topic. This topic is expected to provide a platform for advancing research on the deep understanding the inflammatory mechanisms of electrophysiology. Regarding clinical translation, innovative immunoregulation strategies that manipulate immune cells to resolve inflammation for the management of arrhythmias in cardiovascular diseases will be explored. Additionally, the application of rationally designed nanoparticles or biomaterials that initiate or induce immune modulation to inhibit the activation of inflammation signaling pathways will be examined.
We welcome submissions on the following topics but are not limited to:
- Exploring the interactions between immune cells and neural systems that influence information transfer, extrapolating findings from the field of neuroscience to the heart and defining common themes.
- Unravelling underlying mechanisms in inflammation-relevant autonomic regulation on arrhythmias in cardiovascular diseases such as myocardial ischemia/infarction, heart failure, autoimmune diseases and myocarditis.
- Unravelling underlying mechanisms in inflammation-relevant ion channel regulation in inflammation-relevant arrhythmias, myocardial ischemia/infarction, heart failure, autoimmune diseases and myocarditis.
- Other mechanism relating electrophysiology character: i.e. membrane potential, calcium handling, and gap junction coupling etc. and inflammation process.
- Innovative immunoregulation strategies that manipulate immune cells to resolve inflammation for the management of arrhythmias in cardiovascular diseases.
- Application of rationally designed nanoparticles or biomaterials that initiate or induce immune modulation for inhibition of activation of inflammation signaling pathways.
Keywords:
arrhythmogenesis, neuroimmune-inflammation, ion channels, sympathetic nerve, electrical coupling, ion channel, electrophysiological properties, cardiovascular disease (CVD), atrial fibrillation (AF), ventricular tachycardia (VT), immunological therapy
Important Note:
All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.
Changes in the numbers, phenotypes and electrophysiological properties of leukocytes frequently gave rise to arrhythmias, such as atrial fibrillation and ventricular arrhythmia, in patients with myocardial ischemia/infarction, heart failure and myocarditis. Many underlying conditions are associated with the inflammatory component and arrhythmia. For example, macrophages electrotonically couple to cardiomyocytes via connexin 43-containing gap junctions; immune cells interact with neural systems that influence information transfer; cytokines impact ion channel expression and function. These clinical associations between inflammatory indicators and arrhythmia incidence provide molecular insights. mmunotherapy is emerging as a potential treatment option for rhythm disorders, although more exploration is needed in the future. In this topic, we aim to bridge the knowledge gap between electrophysiology and immunology, promote conceptual connections between these two fields and explore promising opportunities for future clinical arrhythmia prevention and therapy.
We aim to discover innovative basic mechanism for clinical cardiac arrhythmias, and explore novel immunotherapy or immunomodulation strategies that can directly resolve immune-related arrhythmias. It is noteworthy that functional mechanism of monocytes, macrophages, natural killer cells, T cells, and other engineered immune cells on electrophysiology character such as autonomic nerve regulation and ion channel regulation are of particularly interest in this research topic. This topic is expected to provide a platform for advancing research on the deep understanding the inflammatory mechanisms of electrophysiology. Regarding clinical translation, innovative immunoregulation strategies that manipulate immune cells to resolve inflammation for the management of arrhythmias in cardiovascular diseases will be explored. Additionally, the application of rationally designed nanoparticles or biomaterials that initiate or induce immune modulation to inhibit the activation of inflammation signaling pathways will be examined.
We welcome submissions on the following topics but are not limited to:
- Exploring the interactions between immune cells and neural systems that influence information transfer, extrapolating findings from the field of neuroscience to the heart and defining common themes.
- Unravelling underlying mechanisms in inflammation-relevant autonomic regulation on arrhythmias in cardiovascular diseases such as myocardial ischemia/infarction, heart failure, autoimmune diseases and myocarditis.
- Unravelling underlying mechanisms in inflammation-relevant ion channel regulation in inflammation-relevant arrhythmias, myocardial ischemia/infarction, heart failure, autoimmune diseases and myocarditis.
- Other mechanism relating electrophysiology character: i.e. membrane potential, calcium handling, and gap junction coupling etc. and inflammation process.
- Innovative immunoregulation strategies that manipulate immune cells to resolve inflammation for the management of arrhythmias in cardiovascular diseases.
- Application of rationally designed nanoparticles or biomaterials that initiate or induce immune modulation for inhibition of activation of inflammation signaling pathways.
Keywords:
arrhythmogenesis, neuroimmune-inflammation, ion channels, sympathetic nerve, electrical coupling, ion channel, electrophysiological properties, cardiovascular disease (CVD), atrial fibrillation (AF), ventricular tachycardia (VT), immunological therapy
Important Note:
All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.