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.