Background::
Cardiac intrinsic autonomic nerve remodelling has been reported
to play an important role in the recurrence of atrial fibrillation after radiofrequency
ablation, which significantly affects the long-term efficacy of this procedure. lncRNAs
have been shown to interact in the pathological processes underlying heart diseases.
However, the roles and mechanisms of lncRNAs in cardiac intrinsic autonomic nerve remodelling
during atrial fibrillation reduction after ganglionated plexus ablation remain
unknown.
Objectives::
The aim of this study was to investigate the mechanism by which lncRNA-
056298 modulates GAP43 to affect cardiac intrinsic autonomic nerve remodelling
and facilitate the induction of atrial fibrillation after ganglionated plexus ablation.
Methods::
A canine model of right atrial ganglionated plexus ablation was established.
The atrial electrophysiological characteristics and neural markers were detected before
and after 6 months of ganglionated plexus ablation. High-throughput sequencing was
used to screen differentially expressed lncRNAs in target atrial tissues, and lncRNA-
056298 was selected to further explore its effects and mechanisms on cardiac intrinsic
autonomic nerve remodelling.
Results::
The induction rate of atrial fibrillation increased in dogs after ganglionated
plexus ablation. Overexpression of lncRNA-056298 by lentivirus can shorten the atrial
effective refractory period and increase the induction of atrial fibrillation. lncRNA-
056298 promoted cardiac intrinsic autonomic nerve remodelling via endogenous
competition with cfa-miR-185 to induce transcription of its target gene GAP43, thereby
affecting the induction of atrial fibrillation.
Conclusions::
lncRNA-056298 regulates GAP43 by sponging miR-185, which affects
cardiac intrinsic autonomic nerve remodelling and mediates atrial fibrillation induction
after ganglionated plexus ablation.