title: Atrial Calpains: Mediators of Atrialmyopathies in Atrial Fibrillation.
abstract: 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 AF.
authors.affiliation: EUTRAF Working Group: Molecular Electrophysiology, University Hospital Magdeburg, Germany.
authors.forename: Alicja
authors.initials: A
authors.lastname: Bukowska
authors.affiliation: Institute of Medical Biochemistry and Molecular Biology, Ernst-Moritz-Arndt University,Greifswald, Germany.
authors.forename: Uwe
authors.initials: U
authors.lastname: Lendeckel
authors.affiliation: EUTRAF Working Group: Molecular Electrophysiology, University Hospital Magdeburg, Germany; Department of Cardiology and Intensive Care Medicine, St. Vincenz-Hospital, Paderborn,Germany.
authors.forename: Andreas
authors.initials: A
authors.lastname: Goette
keywords: Atrial fibrillation; Calcium; Calpain; Pathophysiology; Protease