The IL-33/ST2 pathway, inflammation and atherosclerosis: Trigger and target?

The “inflammatory hypothesis” of atherosclerosis postulates that inflammatory cell signalling drives the formation, growth and ultimately the instability of atherosclerotic plaques, setting up the substrate for the thrombotic response that causes myocardial damage or infarction. The recent Canakinum ab Antiinflammatory Thrombosis Outcome Study (CANTOS) trial has been hailed as the first demonstration, ex iuvantibus, of the inflammatory hypothesis. Indeed, interleukin (IL)-1β inhibition was found to reduce cardiovascular events in patients with previous myocardial infarction and raised high-sen sitivity C-reactive protein, despite no effects on the lipid profile.
Source: International Journal of Cardiology - Category: Cardiology Authors: Source Type: research