4.1 Major findings
The findings presented in this study
demonstrate
that isorhamnetin suppresses AngII-induced AF
vulnerability
through the
inhibition
of electrical and structural remodeling. Isorhamnetin
alleviates
abnormal
diastolic
intracellular
Ca2+ activities by modulating CaMKII-mediated RyR2 and
restores aberrant AP morphology via the regulation of Cav1.2 activation
in reverse electrical remodeling.
In addition, isorhamnetin prevents left atrial enlargement and severe
fibrosis via the abrogation of TRPC-mediated MAPK and TGF-β pathways in
reverse structural remodeling. To the best of our
knowledge,
this study is the first to investigate the potential mechanism by which
natural flavonoids suppress vulnerability to
AF.