[Research progress on the mechanism of NLRP3 inflammasome in new-onset fibrillation in sepsis].

Abstract

Patients with new-onset atrial fibrillation in sepsis have a high mortality rate and poor prognosis. At present, the pathogenesis of new-onset atrial fibrillation in sepsis has not been fully elucidated. Studies have shown that both sepsis and atrial fibrillation are closely related to NOD-like receptor protein 3 (NLRP3). NLRP3 inflammasome can not only induce the activation of caspase-1 and the subsequent release of cellular pro-inflammatory factors, but also participate in the occurrence and development of sepsis and promote the occurrence and development of atrial fibrillation. It is concluded that the NLRP3 inflammasome may play an important role in the occurrence and development of new-onset atrial fibrillation in sepsis. This paper summarized the current research progress on the structure and function of the NLRP3 inflammasome, its role in sepsis, its mechanism in promoting atrial fibrillation, the relationship between the NLRP3 inflammasome and new-onset atrial fibrillation in sepsis, the feasibility of studying new-onset atrial fibrillation in sepsis, and potential therapeutic targets for new-onset atrial fibrillation in sepsis. This review aims to provide a theoretical basis for future research on the mechanisms by which the NLRP3 inflammasome promotes new-onset atrial fibrillation in sepsis and possible therapeutic targets.