Ca 2+ /Calmodulin-Dependent Protein Kinase II and Protein Kinase A Differentially Regulate Sarcoplasmic Reticulum Ca 2+ Leak in Human Cardiac Pathology
Author(s) -
Thomas H. Fischer,
Jonas Herting,
Theodor Tirilomis,
André Renner,
Stefan Neef,
Karl Toischer,
David Ellenberger,
Anna Förster,
Jan D. Schmitto,
Jan Gummert,
Friedrich A. Schöndube,
Gerd Hasenfuß,
Lars S. Maier,
Samuel Sossalla
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.113.001746
Subject(s) - ryanodine receptor 2 , calmodulin , medicine , ryanodine receptor , endocrinology , protein kinase a , endoplasmic reticulum , muscle hypertrophy , phosphorylation , kinase , calcium , biology , microbiology and biotechnology
Sarcoplasmic reticulum (SR) Ca(2+) leak through ryanodine receptor type 2 (RyR2) dysfunction is of major pathophysiological relevance in human heart failure (HF); however, mechanisms underlying progressive RyR2 dysregulation from cardiac hypertrophy to HF are still controversial.
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