Atrial fibrillation (AF) is
associated with substantial structural changes at cell and tissue level.
Cellular hypertrophy, disintegration of sarcomeres, mitochondrial swelling and
apoptosis have been described as typical histo-morphologic alterations in AF.
Main initiators for cellular alterations in fibrillating atrial myocytes are
cytosolic calcium overload and oxidative stress. Calpains are intracellular Ca2+-
activated proteases and important mediators of calcium overload. Activation of
calpains and down-regulation of the calpain inhibitor, calpastatin, contribute
to myocardial damage in fibrillating atria. Thus, deregulations of the
expression, activity, or subcellular localization of calpain within atrial
myocytes have been established as important mediators of atrial myopathy during
Credits: Alicja Bukowska; Uwe Lendeckel; Andreas Goette