Work

Inflammasome, pyroptosis, and cytokines in myocardial ischemia-reperfusion injury

Year: 2018

Type: article

Abstract: Myocardial ischemia-reperfusion injury induces a sterile inflammatory response, leading to further injury that contributes to the final infarct size. Locally released danger-associated molecular patterns lead to priming and triggering of the NOD-like receptor protein 3 inflammasome and amplification of the inflammatory response and cell death by activation of caspase-1. We review strategies inhibiting priming, triggering, or caspase-1 activity or blockade of the inflammasome-related cytokines interleukin-1β and interleukin-18, focusing on the beneficial effects in experimental models of acute myocardial infarction in animals and the initial results of clinical translational research trials.

Source: American Journal of Physiology-Heart and Circulatory Physiology

DOI: 10.1152/ajpheart.00158.2018

Authors: Stefano Toldo, Adolfo G. Mauro, Zachary Cutter, Antonio Abbate

Institutions: Virginia Commonwealth University, Virginia Commonwealth University Medical Center

Language: English

Topic: Inflammasome and immune disorders

Subfield: Molecular Biology

Field: Biochemistry, Genetics and Molecular Biology

Domain: Life Sciences

SDG: Good health and well-being

Open Access status: bronze

Funder: National Heart, Lung, and Blood Institute