Extracellular Mediators in Atherosclerosis and Thrombosis
This issue of Arteriosclerosis, Thrombosis, and Vascular Biology includes an elegant review titled “Vascular Inflammation and the Renin-Angiotensin System” by Brasier et al.1 This is the first in a series of articles on extracellular mediators in atherosclerosis and thrombosis. The articles in this series will focus on both molecular mediators and cellular effectors that modulate vascular function and lead to thrombosis and atherogenesis. Leaders in the field will contribute their thoughts on the renin-angiotensin system, thrombin, plasminogen activator inhibitor-1, and integrins; on the role of genetically engineered mice in understanding these processes; on platelets, monocytes, and other cellular mediators; and on themes such as molecular signaling and oxidative stress that are of importance across the field.
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The notion that inflammation and arterial thrombosis are interrelated is not new. Indeed, Osler and colleagues2 pontificated on this possibility in research articles and textbooks dating back to the early 20th century. Interestingly, their focus was on inflammation related to infection or to autoimmune diseases and the associated arteritis and thrombotic events that accompanied those syndromes. In that day, it was uncertain whether arterial thrombosis caused myocardial infarction. Beginning in the early 1970s, with angiographic evidence that acute myocardial infarction most often was the result of thrombotic occlusion of the infarct-related artery, the paradigm shifted toward studies of the factors that promote and inhibit thrombosis and plaque rupture. In the past decade, the field has advanced toward an understanding that inflammatory mediators and cells play critical roles in plaque rupture and the ensuing activation of the thrombotic cascade.
We are excited to begin this series with the current review. Although once thought to only be involved in regulation of blood pressure, it is now clear that the renin-angiotensin system regulates vascular function and atherogenesis. It’s a great beginning for what will be an exciting series.