GJA1 and chronic kidney disease: In the present study, we combine in vivo and in vitro models of CKD to investigate if targeting Cx43 expression and hemichannel activity through genetic and pharmacological blockade, could negate loss of markers linked with tubular injury, ultimately improving function through diminished hemichannel activity, restoration of E-cadherin mediated cell-cell adhesion and reduced paracellular permeability.