Oxidized Ca 2+ /Calmodulin-Dependent Protein Kinase II Triggers Atrial Fibrillation
Author(s) -
Anil Purohit,
Adam G. Rokita,
Xiaoqun Guan,
Biyi Chen,
Olha M. Koval,
Niels Voigt,
Stefan Neef,
Thomas Sowa,
Zhan Gao,
Elizabeth D. Luczak,
Hrafnhildur Stefansdottir,
Andrew C. Behunin,
Na Li,
Ramzi El Accaoui,
Baoli Yang,
Paari Dominic Swaminathan,
Robert M. Weiss,
Xander H.T. Wehrens,
LongSheng Song,
Dobromir Dobrev,
Lars S. Maier,
Mark E. Anderson
Publication year - 2013
Publication title -
circulation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.795
H-Index - 607
eISSN - 1524-4539
pISSN - 0009-7322
DOI - 10.1161/circulationaha.113.003313
Subject(s) - reactive oxygen species , angiotensin ii , medicine , endocrinology , genetically modified mouse , calmodulin , sinus rhythm , atrial fibrillation , protein kinase a , renin–angiotensin system , transgene , kinase , receptor , biochemistry , chemistry , calcium , gene , blood pressure
Atrial fibrillation (AF) is a growing public health problem without adequate therapies. Angiotensin II and reactive oxygen species are validated risk factors for AF in patients, but the molecular pathways connecting reactive oxygen species and AF are unknown. The Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) has recently emerged as a reactive oxygen species-activated proarrhythmic signal, so we hypothesized that oxidized CaMKIIδ could contribute to AF.
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