Innate inflammation as the common pathway of risk factors leading to TIAs and stroke.
In the early moments of ischemic stroke, the processes of thrombosis, ischemia, and inflammation are intimately interrelated, setting in motion an injury that leads to infarction and permanent damage. Of these, the potential roles that innate inflammation can play in the evolution of brain tissue damage in response to the ischemic injury are not well understood. Observations in the settings of atherosclerotic cardiovascular disease and cerebral ischemia have much to teach each other. The following provides an introductory overview of the conference "Innate Inflammation as the Common Pathway of Risk Factors Leading to Transient Ischemic Attacks and Stroke: Pathophysiology and Potential Interventions," which took place May 9-10, 2010 at the New York Academy of Sciences. This meeting was convened to explore aspects of the cellular and tissue responses to innate inflammation. A faculty of leading experts was assembled to discuss the role of inflammation in laboratory models of stroke and myocardial infarction, define possible novel means from laboratory evidence to alleviate or prevent inflammation underlying stroke and cardiovascular disease, and present information on current examples of clinical translation of these understandings in relation to human stroke and myocardial infarction.
Division of Hematology, Department of Medicine, University of Washington School of Medicine, Seattle, Washington 98104, USA. grgdlzop@u.washington.edu
Gregory J
GJ
del Zoppo
Philip B
PB
Gorelick
D000818:Animals; D006801:Humans; D007113:Immunity, Innate; D007249:Inflammation / Q000150:complications* / Q000503:physiopathology; D002546:Ischemic Attack, Transient / Q000209:etiology*; D012307:Risk Factors; D020521:Stroke / Q000209:etiology*