AIMS: The present study was designed to investigate whether the beneficial 
effects of beta-blocker propranolol are related to regulation of microRNA miR-1.
METHODS AND RESULTS: We demonstrated that propranolol reduced the incidence of 
arrhythmias in a rat model of myocardial infarction by coronary artery 
occlusion. Overexpression of miR-1 was observed in ischaemic myocardium and 
strikingly, administration of propranolol reversed the up-regulation of miR-1 
nearly back to the control level. In agreement with its miR-1-reducing effect, 
propranolol relieved myocardial injuries during ischaemia, restored the membrane 
depolarization and cardiac conduction slowing, by rescuing the expression of 
inward rectifying K(+) channel subunit Kir2.1 and gap junction channel connexin 
43. Our results further revealed that the beta-adrenoceptor-cAMP-Protein Kinase 
A (PKA) signalling pathway contributed to the expression of miR-1, and serum 
response factor (SRF), which is known as one of the transcriptional enhancers of 
miR-1, was up-regulated in ischaemic myocardium. Moreover, propranolol inhibited 
the beta-adrenoceptor-cAMP-PKA signalling pathway and suppressed SRF expression.
CONCLUSION: We conclude that the beta-adrenergic pathway can stimulate 
expression of arrhythmogenic miR-1, contributing to ischaemic arrhythmogenesis, 
and beta-blockers produce their beneficial effects partially by down-regulating 
miR-1, which might be a novel strategy for ischaemic cardioprotection.