CaMKII and stress mix it up in mitochondria

CaMKII is a newly discovered resident of mitochondria in the heart. Mitochondrial CaMKII promotes poor outcomes after heart injury from a number of pathological conditions, including myocardial infarction (MI), ischemia reperfusion (IR), and stress from catecholamine stimulation. A study using the i...

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Published inFrontiers in pharmacology Vol. 5; p. 67
Main Authors Joiner, Mei-Ling A, Koval, Olha M
Format Journal Article
LanguageEnglish
Published Switzerland Frontiers Media S.A 01.05.2014
Subjects
CaMKII
CaMKIIN
Cell Death
Mitochondria
mitochondrial Calcium uniporter
Pharmacology
mitochondrial calcium uniporter
CaMKII
cell death
CaMKIIN
mitochondria
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Summary:CaMKII is a newly discovered resident of mitochondria in the heart. Mitochondrial CaMKII promotes poor outcomes after heart injury from a number of pathological conditions, including myocardial infarction (MI), ischemia reperfusion (IR), and stress from catecholamine stimulation. A study using the inhibitor of CaMKII, CaMKIIN, with expression delimited to myocardial mitochondria, indicates that an underlying cause of heart disease results from the opening of the mitochondrial permeability transition pore (mPTP). Evidence from electrophysiological and other experiments show that CaMKII inhibition likely suppresses mPTP opening by reducing Ca(2+) entry into mitochondria. However, we expect other proteins involved in Ca(2+) signaling in the mitochondria are affected with CaMKII inhibition. Several outstanding questions remain for CaMKII signaling in heart mitochondria. Most importantly, how does CaMKII, without the recognized N-terminal mitochondrial targeting sequence transfer to mitochondria?
Bibliography:ObjectType-Article-2
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Reviewed by: David A. Brown, East Carolina University, USA; Andrew G. Edwards, Oslo University Hospital and Simula Research Laboratory, Norway; Jeffrey R. Erickson, University of Otago, New Zealand
Edited by: Andrew G. Edwards, Oslo University Hospital and Simula Research Laboratory, Norway
This article was submitted to Pharmacology of Ion Channels and Channelopathies, a section of the journal Frontiers in Pharmacology.
ISSN:1663-9812
1663-9812
DOI:10.3389/fphar.2014.00067