Vascular cells (which include endothelial cells, ECs; smooth muscle cells, SMCs; and pericytes) are an essential constituent of vasculature and are involved in the modulation of vascular tone and blood pressure. Emerging studies have demonstrated that mechanical sensation following calcium signaling is significant in determining vascular health fate. Moreover, transient receptor potential (TRP) channels and Piezo channels are non-selective cationic channels permeable to Ca2+, and their gating can be stimulated by various mechanical stimuli, including membrane stretching, compression, or shear stress. Dysregulation of vascular cells is critically involved in cardiovascular diseases, such as atherosclerosis, myocardial infarction, hypertension, pulmonary hypertension, hypertrophic heart disease, and heart failure.
Recent advances in cell mechanobiology have profoundly impacted our understanding of the physiological and pathophysiological role of mechanosensitive ion channels in the vascular system. Mechanosensitive ion channels are mediators of blood flow and maintain vascular function. Moreover, aberrant mechanotransduction can alter cellular crosstalk dynamics which affect gene expression leading to changes in vascular cell function, and vessel remodeling. While it is clear that the variety of mechanical stimuli and mechanosensitive channels in the vasculature are of great physiological importance in cardiovascular homeostasis, how they interact among pathways and other mechanosensory components remains a question.
The overall goal of this Research Topic is to showcase novel and multifaceted research approaches toward exploring underlying cellular and molecular mechanisms of mechanotransduction, and calcium signaling in health and disease conditions. We expect that this research topic will 1) address essential questions that further our understanding, 2) identify gaps in our knowledge that will ultimately lead to future research directions, and 3) make potential therapeutic strategies for treating vascular diseases.
We encourage submissions of reviews, mini-reviews, brief research reports, methods, and original research articles focusing on (but not limited to) the following topics:
• The mechanosensitive regulators in the pathogenesis of vascular diseases.
• Mechano‐dependent signaling in blood pressure homeostasis
• Advances in the understanding of Ca2+ signaling and vascular remodeling in hypertension
• Signaling mechanisms of domain regulation in vascular cells
• Crosstalk between vascular cells in vascular disease, especially the involvement of ion channels or gap junctions.
• Novel discoveries of endothelial TRP, and smooth muscle cell TRP ion channels
• Novel discoveries of endothelial and smooth muscle cell piezo1/2 channels .
• Novel studies of fibroblasts in vascular disorders (ex. vascular calcification, enhanced vascular stiffness, and hypercontractility) and diseases.
Vascular cells (which include endothelial cells, ECs; smooth muscle cells, SMCs; and pericytes) are an essential constituent of vasculature and are involved in the modulation of vascular tone and blood pressure. Emerging studies have demonstrated that mechanical sensation following calcium signaling is significant in determining vascular health fate. Moreover, transient receptor potential (TRP) channels and Piezo channels are non-selective cationic channels permeable to Ca2+, and their gating can be stimulated by various mechanical stimuli, including membrane stretching, compression, or shear stress. Dysregulation of vascular cells is critically involved in cardiovascular diseases, such as atherosclerosis, myocardial infarction, hypertension, pulmonary hypertension, hypertrophic heart disease, and heart failure.
Recent advances in cell mechanobiology have profoundly impacted our understanding of the physiological and pathophysiological role of mechanosensitive ion channels in the vascular system. Mechanosensitive ion channels are mediators of blood flow and maintain vascular function. Moreover, aberrant mechanotransduction can alter cellular crosstalk dynamics which affect gene expression leading to changes in vascular cell function, and vessel remodeling. While it is clear that the variety of mechanical stimuli and mechanosensitive channels in the vasculature are of great physiological importance in cardiovascular homeostasis, how they interact among pathways and other mechanosensory components remains a question.
The overall goal of this Research Topic is to showcase novel and multifaceted research approaches toward exploring underlying cellular and molecular mechanisms of mechanotransduction, and calcium signaling in health and disease conditions. We expect that this research topic will 1) address essential questions that further our understanding, 2) identify gaps in our knowledge that will ultimately lead to future research directions, and 3) make potential therapeutic strategies for treating vascular diseases.
We encourage submissions of reviews, mini-reviews, brief research reports, methods, and original research articles focusing on (but not limited to) the following topics:
• The mechanosensitive regulators in the pathogenesis of vascular diseases.
• Mechano‐dependent signaling in blood pressure homeostasis
• Advances in the understanding of Ca2+ signaling and vascular remodeling in hypertension
• Signaling mechanisms of domain regulation in vascular cells
• Crosstalk between vascular cells in vascular disease, especially the involvement of ion channels or gap junctions.
• Novel discoveries of endothelial TRP, and smooth muscle cell TRP ion channels
• Novel discoveries of endothelial and smooth muscle cell piezo1/2 channels .
• Novel studies of fibroblasts in vascular disorders (ex. vascular calcification, enhanced vascular stiffness, and hypercontractility) and diseases.