SRA

Background: Inflammation is closely related to atrial fibrillation (AF), in which macrophages play an important role as immune cells. Recent studies have shown that macrophages participate in the electron conduction in the heart, indicating that they have electrophysiological characteristics. However, whether the electrophysiology of macrophages is associated with AF remained unclear. Methods: In the present study, we investigated the electrophysiological changes in macrophages using patch-clamping after tachypacing to mimic AF. RNA-seq was performed to investigate the expression change of atrial myocytes after tachypacing. Rapid atrial stimulation was performed to measure the AF incidence in macrophages-specific CX43 knockout mice. Results: We found that the APD90 and the ICa,L were reduced. Further, we found that tachypacing atrial myocytes led to the secretion of Wnt 7a, further inhibiting the expression of CACNA1C in macrophages. Moreover, the knockout of CX43 in macrophages decreased the incidence of AF in a chronic inflammation mice model. Conclusion: Altogether, these results demonstrated that the electrophysiology of macrophages was related to the development of AF and might be a potential therapeutic target for AF. Overall design: RNA-seq was performed to investigate the expression change of atrial myocytes after tachypacing.