Role of NLRP3 Inflammasome in Myocardial Ischemia-Reperfusion Injury and Ventricular Remodeling

Figures

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  Figure 1. A dual-signal model mediated the activation process of the nucleotide-binding and oligomerization-like receptor pyrin domain-containing protein 3 (NLRP3) inflammasome. The first step was stimulating promotion of nuclear factor-κB into the nucleus to regulate the transcription and translation of the NLRP gene in the nucleus and release it into the cytoplasm. The second step was divided into the non-canonical caspase-11-mediated and canonical NLRP3 inflammasome-mediated pyroptosis pathways. Adobe Illustrator CC 2019 (Adobe Software, San Jose, California, United States) was used for drawing.

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  Figure 2. Potential sources and consequences of nucleotide-binding and oligomerization-like receptor pyrin domain-containing protein 3 (NLRP3) activation signaling pathway during myocardial ischemia and reperfusion (MI/R). MI/R promotes potassium efflux, which directly increases the expression of NIMA-related kinase 7 (NEK7) to form the NLRP3 complex. MI/R promotes sodium-hydron exchange and sodium-calcium exchange and sarcoplasmic reticulum and endoplasmic reticulum release calcium. Calcium overload causes mitochondrial instability and NLRP3 inflammasome activation. MI/R promotes mitochondrial dysfunction and reactive oxygen species (ROS) production. ROS activates the NLRP3 inflammasomes by regulating nuclear factor-κB, caspase-11, and thioredoxin-interacting protein. Adobe Illustrator CC 2019 (Adobe Software, San Jose, California, United States) was used for drawing.