Diseases affecting the cardiovascular system (CVS) remain the main cause of death in the world. Many physiological functions in the cardiovascular system depend on the variations of intracellular calcium concentration (Ca) and the cellular Ca homeostasis is tightly regulated by Ca handling proteins. In recent years, it has become clear that the Ca homeostasis in cells of the CVS is more complex than initially thought. The nature of Ca signals that regulate CV physiology ranges from transient increases in cytoplasmic Ca that control muscle contraction to local sustained subcellular signals, which regulate the function of single organelles, such as the cell nucleus or mitochondria. Alterations in the functions of Ca handling proteins or Ca buffering proteins have been implicated in the development of diseases affecting the CVS, such as arrhythmias, hypertrophy, heart failure, hypertension, or the cardiovascular complications associated with obesity, type 2 diabetes, thyroid problems, or activation of the immune system. Thus, to understand the transition from normal physiological Ca signaling to alterations in Ca signals that promote diseases, it is key to understand Ca signaling on the molecular level.
Many mechanisms controlling intracellular Ca concentration cannot be repeatedly studied within cells obtained from patients suffering from different comorbidities, therefore animal models or cultured cells are employed to address more specific molecular mechanisms. However, the translation of the results from animal models or cultured cells to human treatment remains difficult. The aim of this Research Topic is to collect recent studies on Ca signaling in the CVS, which highlight molecular mechanisms that lead to cardiovascular diseases. It invites authors to contribute with in vivo studies using animal models, in vitro studies using single cells and in silico simulations addressing Ca signaling. We want to better understand the similarities and differences in Ca regulation between different experimental systems: from human to animal models and cultured cells.
The Research Topic is open to reviews and original research papers presenting basic science and preclinical studies, addressing Ca-dependent mechanisms with roles in the onset and progression of cardiovascular diseases, or CVS alterations with aging, inflammation, metabolic diseases or intoxications. Studies on cardiomyocytes, vascular smooth muscle cells, fibroblasts and endothelial cells as well as resident inflammatory cells are highly encouraged.
Research articles may cover, but are not restricted to, alterations of one or more of the following molecular mechanisms
1. Ion channels and cellular excitability
2. IP3 signaling
3. Ca homeostasis and Ca buffering proteins
4. Excitation contraction coupling
5. Ca-dependent gene transcription
6. Subcellular Ca signaling (nuclear Ca signals, mitochondrial signaling)
7. Calcium signaling in cardiac and vascular fibroblasts
8. Biomarkers and novel therapeutic targets
Diseases affecting the cardiovascular system (CVS) remain the main cause of death in the world. Many physiological functions in the cardiovascular system depend on the variations of intracellular calcium concentration (Ca) and the cellular Ca homeostasis is tightly regulated by Ca handling proteins. In recent years, it has become clear that the Ca homeostasis in cells of the CVS is more complex than initially thought. The nature of Ca signals that regulate CV physiology ranges from transient increases in cytoplasmic Ca that control muscle contraction to local sustained subcellular signals, which regulate the function of single organelles, such as the cell nucleus or mitochondria. Alterations in the functions of Ca handling proteins or Ca buffering proteins have been implicated in the development of diseases affecting the CVS, such as arrhythmias, hypertrophy, heart failure, hypertension, or the cardiovascular complications associated with obesity, type 2 diabetes, thyroid problems, or activation of the immune system. Thus, to understand the transition from normal physiological Ca signaling to alterations in Ca signals that promote diseases, it is key to understand Ca signaling on the molecular level.
Many mechanisms controlling intracellular Ca concentration cannot be repeatedly studied within cells obtained from patients suffering from different comorbidities, therefore animal models or cultured cells are employed to address more specific molecular mechanisms. However, the translation of the results from animal models or cultured cells to human treatment remains difficult. The aim of this Research Topic is to collect recent studies on Ca signaling in the CVS, which highlight molecular mechanisms that lead to cardiovascular diseases. It invites authors to contribute with in vivo studies using animal models, in vitro studies using single cells and in silico simulations addressing Ca signaling. We want to better understand the similarities and differences in Ca regulation between different experimental systems: from human to animal models and cultured cells.
The Research Topic is open to reviews and original research papers presenting basic science and preclinical studies, addressing Ca-dependent mechanisms with roles in the onset and progression of cardiovascular diseases, or CVS alterations with aging, inflammation, metabolic diseases or intoxications. Studies on cardiomyocytes, vascular smooth muscle cells, fibroblasts and endothelial cells as well as resident inflammatory cells are highly encouraged.
Research articles may cover, but are not restricted to, alterations of one or more of the following molecular mechanisms
1. Ion channels and cellular excitability
2. IP3 signaling
3. Ca homeostasis and Ca buffering proteins
4. Excitation contraction coupling
5. Ca-dependent gene transcription
6. Subcellular Ca signaling (nuclear Ca signals, mitochondrial signaling)
7. Calcium signaling in cardiac and vascular fibroblasts
8. Biomarkers and novel therapeutic targets
