Immunometabolism is a field of research that focuses on the interaction between the immune system and metabolism. There is increasing evidence that dysregulation of immunometabolism can contribute to the development of various diseases, including heart failure. Heart failure is a complex clinical syndrome that results from impaired cardiac function, leading to reduced cardiac output and tissue perfusion. The pathophysiology of heart failure involves a complex interplay between multiple factors, including genetics, environmental factors, inflammation, and metabolic dysfunction. Immune cells and metabolic pathways are also involved in the development and progression of heart failure.
Extracellular vesicles (EVs) are small membranous structures released by cells that play important roles in cell-to-cell communication and the transport of various biomolecules. In the context of heart failure, EVs have been found to be involved in several pathological processes. One of the key roles of EVs in heart failure is their contribution to cardiac remodeling. EVs released by cardiac cells, such as cardiomyocytes and fibroblasts, contain various signaling molecules, metabolites and microRNAs that can affect the behavior of other cells in the heart, including immune cells and endothelial cells. These EVs can promote fibrosis, inflammation, and apoptosis, all of which can contribute to the progression of heart failure. In addition, EVs released by circulating cells, such as platelets and leukocytes, can also play a role in heart failure. These EVs can activate endothelial cells, promote inflammation, and contribute to thrombosis, all of which can impair cardiac function.
The main aim of this Research Topic is to better understand the complex interplay between immune cells, metabolic pathways, EVs and microRNA in the context of heart failure, which could lead to the development of new therapies and prevention strategies for this debilitating disease
We welcome the following article types: Original Research, Brief Research Report, Case Report, Clinical Trial, General Commentary, Hypothesis & Theory, Methods, Perspective, Review, Mini Review, Opinion, Study Protocol, and Systematic Review.
We welcome papers focusing on, but not limited to the following themes:
- Immunometabolism and heart failure
- Metabolic basis of trained immunity in cardiovascular diseases
- Extracellular vesicles (EVs) and cardiovascular diseases
- Non-coding RNA, RNA binding proteins and the failing heart
- Cellular crosstalk in cardiovascular diseases
Immunometabolism is a field of research that focuses on the interaction between the immune system and metabolism. There is increasing evidence that dysregulation of immunometabolism can contribute to the development of various diseases, including heart failure. Heart failure is a complex clinical syndrome that results from impaired cardiac function, leading to reduced cardiac output and tissue perfusion. The pathophysiology of heart failure involves a complex interplay between multiple factors, including genetics, environmental factors, inflammation, and metabolic dysfunction. Immune cells and metabolic pathways are also involved in the development and progression of heart failure.
Extracellular vesicles (EVs) are small membranous structures released by cells that play important roles in cell-to-cell communication and the transport of various biomolecules. In the context of heart failure, EVs have been found to be involved in several pathological processes. One of the key roles of EVs in heart failure is their contribution to cardiac remodeling. EVs released by cardiac cells, such as cardiomyocytes and fibroblasts, contain various signaling molecules, metabolites and microRNAs that can affect the behavior of other cells in the heart, including immune cells and endothelial cells. These EVs can promote fibrosis, inflammation, and apoptosis, all of which can contribute to the progression of heart failure. In addition, EVs released by circulating cells, such as platelets and leukocytes, can also play a role in heart failure. These EVs can activate endothelial cells, promote inflammation, and contribute to thrombosis, all of which can impair cardiac function.
The main aim of this Research Topic is to better understand the complex interplay between immune cells, metabolic pathways, EVs and microRNA in the context of heart failure, which could lead to the development of new therapies and prevention strategies for this debilitating disease
We welcome the following article types: Original Research, Brief Research Report, Case Report, Clinical Trial, General Commentary, Hypothesis & Theory, Methods, Perspective, Review, Mini Review, Opinion, Study Protocol, and Systematic Review.
We welcome papers focusing on, but not limited to the following themes:
- Immunometabolism and heart failure
- Metabolic basis of trained immunity in cardiovascular diseases
- Extracellular vesicles (EVs) and cardiovascular diseases
- Non-coding RNA, RNA binding proteins and the failing heart
- Cellular crosstalk in cardiovascular diseases