Figure 1: The figure represents a simplified scheme of events occurring during AMI leading to IL-1 mediated sterile inflammation. Acute myocardial ischemia leads to ischemic necrosis of cardiomyocytes. Necrotic cells release Interleukin-1α (IL-1α), ATP, and other Danger Associated Molecular Patterns (DAMPs) that in turn activate the Interleukin-1 receptor (IL-1RI)/Interleukin-1 receptor associated protein (IL-1RAcP), the purinergic receptor P2X7, and the Toll-like receptors (TLRs), respectively. Leukocytes respond to the pro-inflammatory stimuli forming the inflammasome and actively producing IL-1β, which is released through a P2X7 mediated mechanism. The IL-1β released binds to the IL-1RI through an autocrine/paracrine fashion, amplifying the inflammatory response in leukocytes and promoting programmed cell death (apoptosis) and contractile dysfunction in cardiomyocytes. Potential therapeutic anti-IL-1 strategies (highlighted as ø in the figure) include inhibition or blockade of IL-1α, IL-1β, IL-1RI, IL-1RAcP, P2X7, TLRs, caspase-1, cryopyrin (or other members of the inflammasome), NFκB (or other proinflammatory transcription factors).