The massive cell death that occurs during myocardial infarction releases self-DNA and triggers an interferon response in infiltrating leukocytes via a cGAS–STING–IRF3 pathway. Interference with this response—either by genetic disruption of the pathway or antibody blockade of the type I interferon receptor—is beneficial in mice subjected to myocardial infarction.
- Kevin R King
- Aaron D Aguirre
- Ralph Weissleder