About this Research Topic
This is a Research Topic initiated by NAVBO, the North American Vascular Biology Organization.
Extracellular vesicles (EV) are small, membranous entities released by a variety of cell types to participate in a multitude of physiological and pathophysiological processes within a tissue and in circulation. Their cargo consists of proteins and microRNAs allowing them to interact with both cells and the extracellular matrix. In the cardiovascular system, EVs contribute to both inflammation- and calcification-associated processes. EV-mediated cardiovascular calcification poses a crucial mechanism in the onset and progression of atherosclerosis and calcific aortic valve disease, functioning as a fuse and a driving force for both inflammatory and fibrocalcific responses. Recent discoveries spurred by the rise of multi-omics have led to a more profound understanding of the molecular mechanisms of calcifying EV formation and release by vascular/valvular wall cells, endothelial cells and inflammatory cells. Herein, EVs assume a dual role as ignition foci of calcification and as intercellular communicators to induce a pro-inflammatory and/or pro-osteogenic phenotype.
Despite recent advancements in vesicle biology in the context of cardiovascular pathologies, current therapeutic regimen in atherosclerotic and calcific valve disease are still devoid of causative strategies to prevent the onset or inhibit progression of calcification and inflammation. Furthermore, current imaging modalities fall short of detecting early, subclinical calcification in vivo, delaying diagnosis and therapy of already progressing pathological processes. We aim to gain a full understanding of the mechanisms driving EV-mediated formation of microcalcification, its progression to macrocalcification, and the concomitant EV-induced inflammatory response in cardiovascular tissues. For this purpose, our work is intended to further divulge the role of EVs in genesis and growth of calcification and the tissue inflammatory response. Groundbreaking advances in imaging modalities, multi-omics, systems biology, data science and more are necessary to unveil the mechanisms and regulatory pathways involved in the intricate balance of EV-mediated inflammation and the formation of macro- or microcalcification controlling structural stability of cardiovascular tissues. The research topic editors pioneered the paradigm of an EV-centered approach in the pathophysiology of cardiovascular calcification and inflammation, thereby striving to identify EV-bound molecular targets for a potential new generation of drug therapies to combat cardiovascular disease.
Themes we would like authors to address include, but are not limited to:
1) Experimental studies on the regulatory mechanisms of extracellular vesicle release in the context of atherosclerosis/valve disease/heart failure.
2) Discovery of EV-bound targets of intercellular communication, mediators inducing/inhibiting osteogenic differentiation/proinflammatory phenotype.
3) Studies involving EVs released by monocytes/macrophages, the role of EVs in the cardiovascular inflammatory response.
4) Multi-omics: secretomics, vesicle-omics of different cell populations and disease models.
5) Translational studies on circulating EVs, EV-bound blood biomarkers in health and disease states.
Extracellular vesicles (EV) are small, membranous entities released by a variety of cell types to participate in a multitude of physiological and pathophysiological processes within a tissue and in circulation. Their cargo consists of proteins and microRNAs allowing them to interact with both cells and the extracellular matrix. In the cardiovascular system, EVs contribute to both inflammation- and calcification-associated processes. EV-mediated cardiovascular calcification poses a crucial mechanism in the onset and progression of atherosclerosis and calcific aortic valve disease, functioning as a fuse and a driving force for both inflammatory and fibrocalcific responses. Recent discoveries spurred by the rise of multi-omics have led to a more profound understanding of the molecular mechanisms of calcifying EV formation and release by vascular/valvular wall cells, endothelial cells and inflammatory cells. Herein, EVs assume a dual role as ignition foci of calcification and as intercellular communicators to induce a pro-inflammatory and/or pro-osteogenic phenotype.
Despite recent advancements in vesicle biology in the context of cardiovascular pathologies, current therapeutic regimen in atherosclerotic and calcific valve disease are still devoid of causative strategies to prevent the onset or inhibit progression of calcification and inflammation. Furthermore, current imaging modalities fall short of detecting early, subclinical calcification in vivo, delaying diagnosis and therapy of already progressing pathological processes. We aim to gain a full understanding of the mechanisms driving EV-mediated formation of microcalcification, its progression to macrocalcification, and the concomitant EV-induced inflammatory response in cardiovascular tissues. For this purpose, our work is intended to further divulge the role of EVs in genesis and growth of calcification and the tissue inflammatory response. Groundbreaking advances in imaging modalities, multi-omics, systems biology, data science and more are necessary to unveil the mechanisms and regulatory pathways involved in the intricate balance of EV-mediated inflammation and the formation of macro- or microcalcification controlling structural stability of cardiovascular tissues. The research topic editors pioneered the paradigm of an EV-centered approach in the pathophysiology of cardiovascular calcification and inflammation, thereby striving to identify EV-bound molecular targets for a potential new generation of drug therapies to combat cardiovascular disease.
Themes we would like authors to address include, but are not limited to:
1) Experimental studies on the regulatory mechanisms of extracellular vesicle release in the context of atherosclerosis/valve disease/heart failure.
2) Discovery of EV-bound targets of intercellular communication, mediators inducing/inhibiting osteogenic differentiation/proinflammatory phenotype.
3) Studies involving EVs released by monocytes/macrophages, the role of EVs in the cardiovascular inflammatory response.
4) Multi-omics: secretomics, vesicle-omics of different cell populations and disease models.
5) Translational studies on circulating EVs, EV-bound blood biomarkers in health and disease states.
Keywords: extracellular vesicles, vascular calcification, calcific aortic valve disease, coronary artery disease, atherosclerosis, inflammation, Society affiliation RT
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