NLRP3 and atrial fibrillation: Thereafter, Zuo et al. [47] demonstrated that by autophagic degradation through K48- and K63-linked ubiquitylation, SCFAs could halt NLRP3 inflammasome activation via G protein-coupled receptor 43 (GPR43) in both mice and HL-1 cells, and thus exert a protective role on AF.