Possible protective effect of resolvin D1 on inflammation in atrial fibrillation: involvement of ER stress mediated the NLRP3 inflammasome pathway.

Abstract

Atrial fibrillation (AF) is the most common type of cardiac rhythm disturbance. At the cellular level, excessive ROS generation during AF is associated with ER stress, which induces an inflammatory response by activating the unfolded protein response (UPR) pathway and the nuclear factor-kappa B (NF-kB) signaling pathway. Activation of the NLR family pyrin domain containing 3 (NLRP3) inflammasome has been linked to the pathogenesis of AF through NF-kB activation and inflammatory cytokine secretion. It has been shown that NLRP3 inflammasome activation by endoplasmic reticulum (ER) stress is dependent on NF-kB activation. The anti-inflammatory role of resolvin D1 (RvD1), a pro-resolving mediator derived from omega-3 fatty acids, has demonstrated that the NF-κB/NLRP3 inflammasome pathway in different tissues is attenuated after treatment with RvD1. However, the mechanism of the anti-inflammatory activity of RvD1 in AF has not been clarified. This review suggests that RvD1 may inhibit ER stress-induced NLRP3 inflammasome through suppressing NF-κB in cardiac tissue and, thus ameliorate AF.