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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 

No loss of cardioprotection by postconditioning in connexin 43-deficient mice.

In situ hearts and isolated cardiomyocytes from heterozygous connexin 43-deficient ( Cx43(+/-)) mice cannot be protected by ischemic preconditioning or diazoxide. We have now addressed the role of connexin 43 in ischemic postconditioning (PC). Wild type (WT) and Cx43(+/-)mice were subjected to 30 min coronary occlusion and 120 min reperfusion, with and without a PC protocol of three cycles of 10 s coronary occlusion/10 s reperfusion. Infarct size (TTC staining) was reduced by PC from 54+/-5 to 37+/-3% of area at risk in WT. Likewise, infarct size was reduced by PC from 53+/-4 to 34+/-3% of area at risk in Cx43(+/-). We conclude that connexin 43 is no prerequisite for PC's protection. To this end, the signal transduction of ischemic preconditioning and postconditioning differs.[1]

References

  1. No loss of cardioprotection by postconditioning in connexin 43-deficient mice. Heusch, G., Büchert, A., Feldhaus, S., Schulz, R. Basic Res. Cardiol. (2006) [Pubmed]
 
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