Atrial fibrillation (AF) is the most common cardiac arrhythmia in adults. In the coming years and decades, the prevalence and incidence of AF will further increase. The AF-associated pathomechanisms are not yet completely researched. Current therapeutic approaches are effective just for a limited time, associated with severe side effects and may alleviate symptoms, but cannot stop the progression of the disease. Therefore, it is necessary to promote further investigations in cell regulation and cell communication to increase the knowledge of development, progression, and reversibility of AF-associated remodeling processes and to identify new points of therapeutic intervention. AF-induced atrial remodeling processes are mainly caused by reversible changes in protein phosphorylation. In previous work of the laboratory, phosphoproteomic analyses revealed proteins in HL-1 cells that were noticeably differentially regulated after rapid pacing (RP). In this work, these proteins were analyzed and verified in mRNA and protein levels after continuous and interval RP of HL-1 cells. Comparison of the results of the HL-1 model and the atrial tissue of patients in SR and AF should allow for conclusions to clinically and therapeutically relevant signaling pathways and pathomechanisms in AF. The results proved that RP had no effect on the mRNA expression of DDR2, OBSCN, SGK223, MARK2, and limited effect on JPH2 and GPX1 in HL-1 cells. Only after interval RP, the mRNA level of JPH2 was ...