4.7 Conclusion
Our results revealed that isorhamnetin suppressed AF vulnerability by modulating CaMKII-RyR2 and TRPC-mediated MAPK pathways. Our findings further reveal the therapeutically important regulatory functions of isorhamnetin against Ca2+handling in cardiology. The present study not only highlights the potential of isorhamnetin as an anti-arrhythmogenic pharmaceutical or dietary supplement, but also provides a basal evaluation system to verify the anti-arrhythmic effects of other potential substances. Further studies will be needed to investigate the therapeutic effects of isorhamnetin on AF in clinical settings.