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Literature summary for 2.7.1.91 extracted from

  • Jin, Z.Q.; Karliner, J.S.; Vessey, D.A.
    Ischaemic postconditioning protects isolated mouse hearts against ischaemia/reperfusion injury via sphingosine kinase isoform-1 activation (2008), Cardiovasc. Res., 79, 134-140.
    View publication on PubMed

Application

Application Comment Organism
medicine treatment of wild-type and Sphk1 null mouse hearts by ischaemic postconditioning. Postconditioning consisting of 5 s of ischaemia and 5 s of reperfusion for three cycles after the index ischaemia, protects hearts against ischaemia/reperfusion injury, recovery of left ventricular developed pressure and maximum velocity of increase or decrease of left ventricular pressure are elevated and left ventricular end-diastolicpressure is decreased, infarction size is reduced from 40% in the control group to 29% of the risk area in the postconditioning group. Phosphorylation of Akt and extracellular signal-regulated kinases is increased at 10 min of reperfusion. The protection induced by postconditioning is abolished in Sphk1 null mouse hearts Mus musculus

Organism

Organism UniProt Comment Textmining
Mus musculus
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-
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Source Tissue

Source Tissue Comment Organism Textmining
heart
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Mus musculus
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General Information

General Information Comment Organism
physiological function a short period of ischaemic postconditioning protects wild-type mouse hearts against ischaemia/reperfusion injury. The cardiac protection induced by postcondition is abrogated in SphK1-KO mouse hearts Mus musculus