RNA-seq from the hearts of 7-day-old mice that underwent apical resection and anti-arrhythmic drug treatment

Background: As a biological pump, the heart needs to consume a substantial amount of energy to maintain sustained beating. Myocardial energy metabolism was recently reported to be related to the loss of proliferative capacity in cardiomyocytes (CMs). However, the intrinsic relationship between beating rate and proliferation in CMs and whether energy metabolism can regulate this relationship is not known. In this study, we found that limited heart rate reserve (HRR) induced CM proliferation under physiological conditions and promoted cardiac regenerative repair after myocardial injury. However, the role of HRR in regulating CM proliferation and damaged heart repair has not been explored. Results: We found that the control and isoproterenol groups had more similar transcriptional profiles that clearly differed from those of the five groups treated with each anti-arrhythmic drug and thus were clustered together. With Gene Ontology (GO) analysis, we found that genes that commonly showed upregulated expression in various HRR drug-treated cells were related to proliferation and metabolic regulation, including the cell cycle process, heart process, and nucleoside triphosphate metabolic process, with a particular upregulation of the expression of glucose metabolic genes. 1-day-old neonatal mice that underwent apical resection were injected subcutaneously with anti-arrhythmic drugs (amiodarone, metoprolol, propranolol, lidocaine, ivabradine) or isoproterenol for seven consecutive days.