Inflammasome, pyroptosis, and cytokines in myocardial ischemia-reperfusion injury.
Stefano ToldoAdolfo G MauroZachary CutterAntonio AbbatePublished in: American journal of physiology. Heart and circulatory physiology (2018)
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.
Keyphrases
- inflammatory response
- ischemia reperfusion injury
- cell death
- acute myocardial infarction
- left ventricular
- oxidative stress
- lipopolysaccharide induced
- lps induced
- cell cycle arrest
- toll like receptor
- induced apoptosis
- percutaneous coronary intervention
- signaling pathway
- binding protein
- nlrp inflammasome
- protein protein
- immune response
- single molecule
- endoplasmic reticulum stress
- acute coronary syndrome
- nucleic acid
- label free
- cell proliferation
- pi k akt