CaMKII determines mitochondrial stress responses in heart

Mei-ling A. Joiner (), Olha M. Koval, Jingdong Li, B. Julie He, Chantal Allamargot, Zhan Gao, Elizabeth D. Luczak, Duane D. Hall, Brian D. Fink, Biyi Chen, Jinying Yang, Steven A. Moore, Thomas D. Scholz, Stefan Strack, Peter J. Mohler, William I. Sivitz, Long-Sheng Song and Mark E. Anderson ()
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Mei-ling A. Joiner: Carver College of Medicine, University of Iowa
Olha M. Koval: Carver College of Medicine, University of Iowa
Jingdong Li: Carver College of Medicine, University of Iowa
B. Julie He: Carver College of Medicine, University of Iowa
Chantal Allamargot: University of Iowa Central Microscopy Research Facility, Carver College of Medicine, University of Iowa
Zhan Gao: Carver College of Medicine, University of Iowa
Elizabeth D. Luczak: Carver College of Medicine, University of Iowa
Duane D. Hall: Carver College of Medicine, University of Iowa
Brian D. Fink: Iowa City Veterans Affairs Medical Center
Biyi Chen: Carver College of Medicine, University of Iowa
Jinying Yang: Carver College of Medicine, University of Iowa
Steven A. Moore: Carver College of Medicine, University of Iowa
Thomas D. Scholz: Carver College of Medicine, University of Iowa
Stefan Strack: Carver College of Medicine, University of Iowa
Peter J. Mohler: Carver College of Medicine, University of Iowa
William I. Sivitz: Carver College of Medicine, University of Iowa
Long-Sheng Song: Carver College of Medicine, University of Iowa
Mark E. Anderson: Carver College of Medicine, University of Iowa

Nature, 2012, vol. 491, issue 7423, 269-273

Abstract: Calcium exchange and cardiac stress Increased mitochondrial calcium entry has been implicated in myocardial death, heart failure and related conditions. Here, the authors show that inhibition of the multifunctional Ca2+- and calmodulin-dependent protein kinase II (CaMKII) in a mouse model of ischaemia reperfusion injury reduces infarct size and mitochondrial-triggered cell death and dysfunction. This is due to reduced mitochondrial Ca2+ entry through the mitochondrial calcium uniporter and enhanced Ca2+ tolerance of the mitochondrial permeability transition pore. This suggests that CaMKII inhibition could reduce adverse responses to common forms of pathological myocardial stress.

Date: 2012
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DOI: 10.1038/nature11444

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