The vascular endothelial cells are subjected to hemodynamic forces and respond differently to distinct shear patterns. The characteristics of blood flow include laminar and disturbed flow, and fluid shear stress increases as the flow becomes disturbed. Endothelial cells sense and convert the surrounding mechanical stimuli into biochemical signals, and such mechanotransduction determines the endothelial phenotype and function. Experiments ranging from cell culture to whole animal models have indicated that laminar flow improves endothelial cell homeostasis, whereas disturbed flow leads to endothelial dysfunction, followed by vascular smooth muscle cell proliferation and intimal migration. Therefore, disturbed flow is regarded as atheroprone, whereas laminar flow tends to be atheroprotective. In the face of pathological hemodynamic forces, endothelial cells elicit adaptive changes, leading to vascular dysfunction and diseases. In order to identify potential druggable targets for vascular diseases, it is crucial to understand mechanoregulatory molecular networks of the vascular endothelium. Translational research integrating cell biology and clinical manifestations may help to develop novel therapeutic targeting vascular mechanoregulation.
Upon exposure to pathological mechanical stresses, vascular endothelial cells undergo a series of molecular and cellular processes, leading to endothelial dysfunction. Such endothelial mechanotransduction signaling plays a vital role in the pathogenesis of vasculopathy, such as atherosclerosis, vascular calcification, or hemodialysis vascular access complications. It's crucial to unveil the complex mechanobiology in vascular diseases in order to identify potential druggable targets. Furthermore, clinical imaging-based biomechanical simulations, such as computational fluid dynamics and fluid-structure interaction, are important tools to investigate vessel wall biomechanics at the tissue level and provide a window to understand the in vivo vascular microenvironment. Research on this topic is emerging, including hemodynamic force simulation analysis, mechanosensitive molecule discovery using multi-omics approaches at transcriptional, posttranscriptional, and epigenetic levels, and so on. Multidisciplinary approaches can be used to decipher the endothelial cell mechanosensitive and mechanoresponsive mechanisms. We aim to invite articles focusing on recent research advances in this field, including newly identified molecular mechanisms and potential therapeutic targets.
In this Research Topic, we are interested in Review or Original Research articles that focus on the following themes:
1. Hemodynamic forces on endothelial phenotype and function
2. Mechanosensitive and mechanoresponsive molecules in endothelial dysfunction
3. Multi-omics research on endothelial mechanobiology
4. Mechanoregulatory mechanisms of endothelial cells
5. Hemodynamic forces in the pathogenesis of vascular diseases
6. Endothelial mechanobiology in the pathogenesis of vascular diseases
7. Translational research on hemodynamic force-induced endothelial dysfunction
8. CT/MR imaging-based CFD and FSI analysis in vascular diseases
9. Multidisciplinary integrative research on vascular diseases
*Abbreviations: CT, computed tomography; MR, magnetic resonance; CFD, computational fluid dynamics; FSI, fluid-structure interaction.
The vascular endothelial cells are subjected to hemodynamic forces and respond differently to distinct shear patterns. The characteristics of blood flow include laminar and disturbed flow, and fluid shear stress increases as the flow becomes disturbed. Endothelial cells sense and convert the surrounding mechanical stimuli into biochemical signals, and such mechanotransduction determines the endothelial phenotype and function. Experiments ranging from cell culture to whole animal models have indicated that laminar flow improves endothelial cell homeostasis, whereas disturbed flow leads to endothelial dysfunction, followed by vascular smooth muscle cell proliferation and intimal migration. Therefore, disturbed flow is regarded as atheroprone, whereas laminar flow tends to be atheroprotective. In the face of pathological hemodynamic forces, endothelial cells elicit adaptive changes, leading to vascular dysfunction and diseases. In order to identify potential druggable targets for vascular diseases, it is crucial to understand mechanoregulatory molecular networks of the vascular endothelium. Translational research integrating cell biology and clinical manifestations may help to develop novel therapeutic targeting vascular mechanoregulation.
Upon exposure to pathological mechanical stresses, vascular endothelial cells undergo a series of molecular and cellular processes, leading to endothelial dysfunction. Such endothelial mechanotransduction signaling plays a vital role in the pathogenesis of vasculopathy, such as atherosclerosis, vascular calcification, or hemodialysis vascular access complications. It's crucial to unveil the complex mechanobiology in vascular diseases in order to identify potential druggable targets. Furthermore, clinical imaging-based biomechanical simulations, such as computational fluid dynamics and fluid-structure interaction, are important tools to investigate vessel wall biomechanics at the tissue level and provide a window to understand the in vivo vascular microenvironment. Research on this topic is emerging, including hemodynamic force simulation analysis, mechanosensitive molecule discovery using multi-omics approaches at transcriptional, posttranscriptional, and epigenetic levels, and so on. Multidisciplinary approaches can be used to decipher the endothelial cell mechanosensitive and mechanoresponsive mechanisms. We aim to invite articles focusing on recent research advances in this field, including newly identified molecular mechanisms and potential therapeutic targets.
In this Research Topic, we are interested in Review or Original Research articles that focus on the following themes:
1. Hemodynamic forces on endothelial phenotype and function
2. Mechanosensitive and mechanoresponsive molecules in endothelial dysfunction
3. Multi-omics research on endothelial mechanobiology
4. Mechanoregulatory mechanisms of endothelial cells
5. Hemodynamic forces in the pathogenesis of vascular diseases
6. Endothelial mechanobiology in the pathogenesis of vascular diseases
7. Translational research on hemodynamic force-induced endothelial dysfunction
8. CT/MR imaging-based CFD and FSI analysis in vascular diseases
9. Multidisciplinary integrative research on vascular diseases
*Abbreviations: CT, computed tomography; MR, magnetic resonance; CFD, computational fluid dynamics; FSI, fluid-structure interaction.
