Therapeutic S100A8/A9 inhibition reduces NADPH oxidase expression, reactive oxygen species production and NLRP3 inflammasome priming in the ischemic myocardium
Oxidative stress and alterations in redox signalling have been implicated in the pathophysiology of myocardial infarction (MI). NADPH oxidase (Nox) is an important source of reactive oxygen species (ROS) in the infarcted myocardium. Alarmin S100A8/A9 amplifies acute myocardial inflammation in MI and has been shown to be a promising therapeutic target to improve cardiac function post-MI. We aimed t
