No place like inflammasome
Researchers at Virginia Commonwealth University have found that inhibiting inflammasome formation with antagonists of the membrane receptor P2X7 could help prevent heart failure following acute myocardial infarction.1 The findings point to a repurposing opportunity for P2X7 antagonists that companies have in the clinic for inflammatory indications.
About one-third of patients with acute myocardial infarction (AMI) go on to develop heart failure.2 Mechanistically, the lack of blood and nutrient supply to the heart tissues after an AMI triggers inflammation, which ultimately leads to cardiac remodeling and dysfunction.
The precise mechanism of cardiac inflammation following AMI was until recently unknown, and efforts to counter inflammation involved generic inhibition of inflammatory cytokines. Early last year, Japanese researchers first reported that inflammasome formation could be responsible for cardiovascular tissue inflammation following AMI.3