Author
Listed:
- 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
Present address: The Dorothy M. Davis Heart and Lung Research Institute, The Ohio State University, Columbus, Ohio 43210, USA.)
- B. Julie He
(Carver College of Medicine, University of Iowa
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
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
Present address: The Dorothy M. Davis Heart and Lung Research Institute, The Ohio State University, Columbus, Ohio 43210, USA.)
- William I. Sivitz
(Carver College of Medicine, University of Iowa
Iowa City Veterans Affairs Medical Center)
- Long-Sheng Song
(Carver College of Medicine, University of Iowa)
- Mark E. Anderson
(Carver College of Medicine, University of Iowa
Carver College of Medicine, University of Iowa)
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.
Suggested Citation
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 & Thom, 2012.
"CaMKII determines mitochondrial stress responses in heart,"
Nature, Nature, vol. 491(7423), pages 269-273, November.
Handle:
RePEc:nat:nature:v:491:y:2012:i:7423:d:10.1038_nature11444
DOI: 10.1038/nature11444
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