About this Research Topic
The profile of plasma lipoproteins is a major determinant of cardiovascular diseases, the world's leading causes of mortality. There is growing knowledge of lipoprotein functions determined by the interaction with vascular cells eliciting pathways, associated with both pro- and anti-atherogenic effects; this interaction is mutual and often synergistic. The concept of quality and functionality of lipoproteins has brought new interpretations and approaches in the management of cardiovascular diseases, especially atherosclerosis.
Detailing how atherogenic lipoproteins - apoB-containing lipoproteins - interact with vascular cells, including monocyte-derived macrophages in the arterial intima and vice-versa, drives the understanding of pathophysiological mechanisms involved in atherosclerotic plaque formation. Furthermore, mechanisms by which lipoproteins, particularly high-density lipoproteins (HDL), interact with atherogenesis-related mechanisms, such as reverse cholesterol transport, nitric oxide synthesis, glucose homeostasis, antioxidant, and anti-inflammatory actions, reinforce the role of these lipoproteins in cell signaling, a role that is not invariably related to their plasma levels. The phenotype and function of plasma lipoproteins are also greatly influenced by cell signaling pathways.
The aim of this Research Topic is to bring together novel, original findings and critical reviews related to the role of lipoproteins in vascular signaling and in the cellular cross talk that modulates atherogenesis, including insights into altered cell signaling triggered by dysfunctional lipoproteins in coronary heart disease, metabolic diseases, and inflammatory conditions.
Areas to be covered in this Research Topic may include, but are not limited to:
• Atherogenic signaling of apoB-containing lipoproteins;
• Antiatherogenic properties of HDL and atherosclerosis;
• HDL dysfunction and cardiovascular risk;
• Proteomics and lipidomics of lipoproteins;
• Cell-signaling and change in plasma lipoproteins;
• Lipoproteins, infection and inflammation.
Detailing how atherogenic lipoproteins - apoB-containing lipoproteins - interact with vascular cells, including monocyte-derived macrophages in the arterial intima and vice-versa, drives the understanding of pathophysiological mechanisms involved in atherosclerotic plaque formation. Furthermore, mechanisms by which lipoproteins, particularly high-density lipoproteins (HDL), interact with atherogenesis-related mechanisms, such as reverse cholesterol transport, nitric oxide synthesis, glucose homeostasis, antioxidant, and anti-inflammatory actions, reinforce the role of these lipoproteins in cell signaling, a role that is not invariably related to their plasma levels. The phenotype and function of plasma lipoproteins are also greatly influenced by cell signaling pathways.
The aim of this Research Topic is to bring together novel, original findings and critical reviews related to the role of lipoproteins in vascular signaling and in the cellular cross talk that modulates atherogenesis, including insights into altered cell signaling triggered by dysfunctional lipoproteins in coronary heart disease, metabolic diseases, and inflammatory conditions.
Areas to be covered in this Research Topic may include, but are not limited to:
• Atherogenic signaling of apoB-containing lipoproteins;
• Antiatherogenic properties of HDL and atherosclerosis;
• HDL dysfunction and cardiovascular risk;
• Proteomics and lipidomics of lipoproteins;
• Cell-signaling and change in plasma lipoproteins;
• Lipoproteins, infection and inflammation.
Keywords: lipoproteins, HDL, vascular signaling, cardiovascular diseases
Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.
