Journal
JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY
Volume 46, Issue 6, Pages 858-866Publisher
ELSEVIER SCI LTD
DOI: 10.1016/j.yjmcc.2008.11.019
Keywords
Mitochondrial K-ATP channel; Protein kinase C; Reactive oxygen species; Permeability transition; Signaling pathways
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Funding
- NHLBI NIH HHS [P01 HL036573, P01 HL036573-160012, R01 HL067842, R01 HL067842-07] Funding Source: Medline
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Mitochondria are central players in the pathophysiology of ischemia-reperfusion. Activation of plasma membrane G-coupled receptors or the Na,K-ATPase triggers cytosolic signaling pathways that result in cardioprotection. Our working hypothesis is that the Occupied receptors migrate to caveolae, where signaling enzymes are scaffolded into signalosomes that bud off the plasma membrane and migrate to mitochondria. The signalosome-mitochondria interaction then initiates intramitochondrial signaling by opening the mitochondrial ATP-sensitive K+ channel (mitoK(ATP)). MitoK(ATP) opening causes an increase in ROS production, which activates mitochondrial protein kinase C epsilon (PKC epsilon), which inhibits the mitochondrial permeability transition (MPT), thus decreasing cell death. We review the experimental findings that bear on these hypotheses and other modes of protection involving mitochondria. Published by Elsevier Inc.
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