Linked Life Data

20562423

Source:http://linkedlifedata.com/resource/pubmed/id/20562423

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2010-9-10
pubmed:abstractText
Multiple cardioprotective signal pathways that are activated by ischaemic preconditioning (IPC) and those by IPC mimetics converge on mitochondria. Recent studies have shown that pools of Akt, protein kinase C-?, extracellular-regulated kinases, glycogen synthase kinase-3beta (GSK-3beta), and hexokinases (HK) I and II, are localized in mitochondria in addition to their pools in the cytosol. Accumulating evidence indicates that such 'mitochondrial protein kinases' receive signals from cytosolic molecules and enhance tolerance of myocytes to injury. Proteomic analyses suggest that these kinases form complexes with each other and with subunit proteins of the mitochondrial permeability transition pore (mPTP). Functional relationships between the protein kinases in mitochondria have not been fully clarified, but GSK-3beta and HKs appear to be at the end of the signal pathways and directly responsible for inhibition of opening of the mPTP and, thus, for myocyte protection from necrosis. In this review, recent findings supporting roles of mitochondrial protein kinases in protection from myocardial necrosis after ischaemia/reperfusion are summarized and discussed.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
1755-3245
pubmed:author
pubmed:issnType
Electronic
pubmed:day
1
pubmed:volume
88
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
7-15
pubmed:meshHeading
pubmed:year
2010
pubmed:articleTitle
Mitochondrial kinase signalling pathways in myocardial protection from ischaemia/reperfusion-induced necrosis.
pubmed:affiliation
Second Department of Internal Medicine, Sapporo Medical University, School of Medicine, Sapporo, Japan. miura@sapmed.ac.jp
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't