Linked Life Data

19162034

Source:http://linkedlifedata.com/resource/pubmed/id/19162034

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2009-5-15
pubmed:abstractText
Mitochondria are equipped with an efficient machinery for Ca(2+) uptake and extrusion and are capable of storing large amounts of Ca(2+). Furthermore, key steps of mitochondrial metabolism (ATP production) are Ca(2+)-dependent. In the field of cardiac physiology and pathophysiology, two main questions have dominated the thinking about mitochondrial function in the heart: 1) how does mitochondrial Ca(2+) buffering shape cytosolic Ca(2+) levels and affect excitation-contraction coupling, particularly the Ca(2+) transient, on a beat-to-beat basis, and 2) how does mitochondrial Ca(2+) homeostasis influence cardiac energy metabolism. To answer these questions, a thorough understanding of the kinetics of mitochondrial Ca(2+) transport and buffer capacity is required. Here, we summarize the role of mitochondrial Ca(2+) signaling in the heart, discuss the evidence either supporting or arguing against the idea that Ca(2+) can be taken up rapidly by mitochondria during excitation-contraction coupling and highlight some interesting new areas for further investigation.
pubmed:grant
pubmed:commentsCorrections
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
1095-8584
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
46
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
767-74
pubmed:dateRevised
2011-11-3
pubmed:meshHeading
pubmed:year
2009
pubmed:articleTitle
Mitochondrial Ca2+ uptake: tortoise or hare?
pubmed:affiliation
Department of Medicine, Division of Cardiology, Johns Hopkins University, Institute of Molecular Cardiobiology, Baltimore, MD 21205-2195, USA. bor@jhmi.edu
pubmed:publicationType
Journal Article