Abstract
In this issue, Brandner et al have extended previous observations on changes in connexin distribution during skin wound healing and have also proposed that keratinocytes grafted into a wound bed might help to reconstitute a tissue gap junction network dominated by connexins 26 and 30 (hyperproliferative connexins). These findings alert us to the possibility that targeting of specific connexins could provide a new approach to improving therapy of acute and chronic skin wounds.
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