This is a Research Topic initiated by
NAVBO, the North American Vascular Biology Organization.
Evidence from basic science and clinical studies has established the role of inflammation in atherosclerosis and vascular disease. No medical therapies other than cholesterol-lowering statins, however, have become available to effectively target the immune system and reduce cardiovascular events. In addition, many patients on potent statins still suffer from acute vascular complications. Such residual risk has driven research efforts to further explore new mechanisms for vascular inflammation. This Research Topic focuses on new trends in vascular inflammation research. We welcome three types of contributions from various disciplines: 1) review articles; 2) original data manuscripts in fundamental basic science, translational medicine, and clinical studies, and 3) reports on new methods.
We hope that our Research Topic will cover various immune cell types and vascular diseases. Multiple types of immune cells appear to participate in the pathogenesis of vascular disease, but as of yet it remains largely unexplored how the interaction of the multiple subsets of inflammatory cells (e.g., pro- vs. anti-inflammatory) in diseased vessels is regulated. The relative contribution of each cell type also may depend on the disease context and stage.
For decades, research efforts have focused on major risk factors of vascular disease and inflammation such as elevated LDL cholesterol, diabetes, and hypertension. Still, what is the role of non-traditional risk factors (e.g., elevated triglycerides, chronic kidney disease, HIV) in vascular inflammation?
Many molecular mechanisms or pathways for vascular inflammation beyond conventional risk factors (e.g., high LDL) have been proposed. Accelerated or impaired functions of each cell type may play a specific role in vascular disease. What are clinical implications of each of the proposed mechanisms? How can they be translated into the clinic? What have we learned about the role of inflammation in vascular diseases or its complications from clinical trials? Some large cardiovascular outcome trials are currently testing the hypothesis that targeting inflammation may reduce CV risk is patients. When these studies are finalized, how would they change the clinical practice?
The scientific community has recognized a gap between basic science research and drug development and global economic challenges in recent years may have further increased this gap. How can we as a medical community overcome this problem? How can we more effectively predict the potential impact of each novel mechanism in the clinic?
We hope many investigators share similar questions with us and will contribute to this Research Topic.