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La proteína quinasa II oxidado Ca2+/calmodulina-dependiente desencadena la fibrilación auricular

Anil Purohit1, Adam G Rokita, Xiaoqun Guan

  • 1Department of Internal Medicine, Division of Cardiovascular Medicine and Cardiovascular Research Center, Carver College of Medicine (A.P., A.G.R., X.G., B.C., O.M.K., Z.G., E.D.L., H.S., A.C.B., R.N.E.-A., P.D.S., R.M.W., L.-S.S., M.E.A.), Department of Obstetrics and Gynecology (B.Y.), and Department of Molecular Physiology and Biophysics (M.E.A.), University of Iowa, Iowa City; Institute of Pharmacology, Faculty of Medicine, University Duisburg-Essen, Essen, Germany, and Division of Experimental Cardiology, Medical Faculty Mannheim, University of Heidelberg, Mannheim, Germany (N.V., D.D.); Cardiology and Pneumology, German Heart Center, University Hospital Goettingen, Goettingen, Germany (S.N., T.S., L.S.M.); and Department of Molecular Physiology and Biophysics, Baylor College of Medicine, Houston, TX (N.L., X.H.T.W.).

Circulation
|September 14, 2013
PubMed
Resumen

La proteína quinasa II oxidada Ca2+/calmodulina-dependiente (CaMKII) está relacionada con la fibrilación auricular (FA). La reducción del CaMKII oxidado puede ofrecer nuevas terapias para los pacientes con AF.

Palabras clave:
La angiotensina II también está presente.las arritmias, las arritmias cardíacas, las arritmias cardíacas.La fibrilación auricular es una fibrilación auricular.La proteína quinasa dependiente de calcio-calmodulina y dependiente de calcio-calmodulina es de tipo II.especies reactivas de oxígeno.

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