Editorial
Stefano Toldo, Eleonora Mez
Abstract
The synthesis and release of Interleukin-1 (IL-1) are finely regulated processes necessary for the initiation of an inflammatory response to injury. Release of IL-1α from injured cells and of mature IL-1β from circulating monocytes initiates the local and systemic inflammatory response, respectively. An intense IL-1-dependent response occurs during Acute Myocardial Infarction (AMI) and promotes Heart Failure (HF). In advanced HF, a chronic IL-1β-dependent process alters cardiovascular function leading to impaired performance, poor quality of life and increased morbidity and mortality. Here in reviewing the evidence in preclinical studies; we discuss potential strategies to disrupt IL-1 signaling in AMI and HF, and review the results of the initial pilot clinical trials.