based on these data it is concluded that in failing hearts , diminished zo-1 expression coincides with reduced connexin 43 staining indicating that zo-1 plays an important role in gap junctional formation and stability .
abstractfocal disorganization of gap junctional distribution and down - regulation of the major gap junctional protein connexin 43 are typical features of myocardial remodelling in the failing human heart . 
 increasing evidence indicates that connexin 43 interacts with zonula - occludens-1 ( zo-1 ) , and it has recently been shown that zo-1 promotes the formation and growth of gap junctional plaques . in the present study , distribution patterns of zo-1 and connexin 43 were studied in normal and in heart failure patients using double - label immunohistochemistry and confocal microscopy . 
 zo-1 was found to be co - localized with connexin 43 at intercalated disks . 
 importantly , in patients with heart failure due to dilated or ischaemic cardimyopathy , areas of diminished connexin 43 expression were characterized by a markedly reduced zo-1 staining . 
 based on these data it is concluded that in patients with heart failure , down - regulation of zo-1 matches the diminished expression levels of connexin 43 , suggesting that zo-1 plays an important role in gap junction formation and gap junction plaque stability .