| http://purl.uniprot.org/citations/15105171 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/15105171 | http://www.w3.org/2000/01/rdf-schema#comment | "The creatine kinase (CK) system is involved in the rapid transport of high-energy phosphates from the mitochondria to the sites of maximal energy requirements such as myofibrils and sarcolemmal ion pumps. Hearts of mice with a combined knockout of cytosolic M-CK and mitochondrial CK (M/Mito-CK(-/-)) show unchanged basal left ventricular (LV) performance but reduced myocardial high-energy phosphate concentrations. Moreover, skeletal muscle from M/Mito-CK(-/-) mice demonstrates altered Ca2+ homeostasis. Our hypothesis was that in CK-deficient hearts, a cardiac phenotype can be unmasked during acute stress conditions and that susceptibility to ischemia-reperfusion injury is increased because of altered Ca2+ homeostasis. We simultaneously studied LV performance and myocardial Ca2+ metabolism in isolated, perfused hearts of M/Mito-CK(-/-) (n = 6) and wild-type (WT, n = 8) mice during baseline, 20 min of no-flow ischemia, and recovery. Whereas LV performance was not different during baseline conditions, LV contracture during ischemia developed significantly earlier (408 +/- 72 vs. 678 +/- 54 s) and to a greater extent (50 +/- 2 vs. 36 +/-3 mmHg) in M/Mito-CK(-/-) mice. During reperfusion, recovery of diastolic function was impaired (LV end-diastolic pressure: 22 +/- 3 vs. 10 +/-2 mmHg), whereas recovery of systolic performance was delayed, in M/Mito-CK(-/-) mice. In parallel, Ca2+ transients were similar during baseline conditions; however, M/Mito-CK(-/-) mice showed a greater increase in diastolic Ca2+ concentration ([Ca2+]) during ischemia (237 +/- 54% vs. 167 +/-25% of basal [Ca2+]) compared with WT mice. In conclusion, CK-deficient hearts show an increased susceptibility of LV performance and Ca2+ homeostasis to ischemic injury, associated with a blunted postischemic recovery. This demonstrates a key function of an intact CK system for maintenance of Ca2+ homeostasis and LV mechanics under metabolic stress conditions."xsd:string |
| http://purl.uniprot.org/citations/15105171 | http://purl.org/dc/terms/identifier | "doi:10.1152/ajpheart.01016.2003"xsd:string |
| http://purl.uniprot.org/citations/15105171 | http://purl.uniprot.org/core/author | "Meyer K."xsd:string |
| http://purl.uniprot.org/citations/15105171 | http://purl.uniprot.org/core/author | "Neubauer S."xsd:string |
| http://purl.uniprot.org/citations/15105171 | http://purl.uniprot.org/core/author | "Wagner H."xsd:string |
| http://purl.uniprot.org/citations/15105171 | http://purl.uniprot.org/core/author | "Boehm E."xsd:string |
| http://purl.uniprot.org/citations/15105171 | http://purl.uniprot.org/core/author | "Spindler M."xsd:string |
| http://purl.uniprot.org/citations/15105171 | http://purl.uniprot.org/core/author | "Stromer H."xsd:string |
| http://purl.uniprot.org/citations/15105171 | http://purl.uniprot.org/core/author | "Leupold A."xsd:string |
| http://purl.uniprot.org/citations/15105171 | http://purl.uniprot.org/core/date | "2004"xsd:gYear |
| http://purl.uniprot.org/citations/15105171 | http://purl.uniprot.org/core/name | "Am J Physiol Heart Circ Physiol"xsd:string |
| http://purl.uniprot.org/citations/15105171 | http://purl.uniprot.org/core/pages | "H1039-45"xsd:string |
| http://purl.uniprot.org/citations/15105171 | http://purl.uniprot.org/core/title | "Creatine kinase-deficient hearts exhibit increased susceptibility to ischemia-reperfusion injury and impaired calcium homeostasis."xsd:string |
| http://purl.uniprot.org/citations/15105171 | http://purl.uniprot.org/core/volume | "287"xsd:string |
| http://purl.uniprot.org/citations/15105171 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/15105171 |
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