Inflammation, Inflammasome Activation, and Atrial Fibrillation

David R Van Wagoner, Mina K Chung, David R Van Wagoner, Mina K Chung

No abstract available

Keywords: C-reactive protein; Editorials; atrial fibrillation; inflammasomes; inflammation; interleukins.

Figures

The NLRP3 receptor is activated in a 2 step process (priming and activation) by many different types of stimuli, ranging from activation of Toll like receptors (TLRs), the IL1 receptor (IL1-R), TNF-receptors (TNFR), and Gq-coupled that promote IP3 production. Endoplasmic reticulum stress associated with obesity, hypoxia and ischemia also activates NLRP3 receptors, resulting in increased IL-1β and IL-18 production. Protein and/or peptide aggregates elicit the unfolded protein response; this promotes autophagy and mitophagy, resulting in impaired mitochondrial function, and reactive oxygen species (ROS) production that increases spontaneous release of calcium from the sarcoplasmic reticulum, contributing to atrial ectopy that can initiate episodes of atrial fibrillation.