GJA1 and Sepsis: For example, in the pulmonary barrier, studies show that during sepsis, lipopolysaccharide (LPS)-induced hyperpermeability is related to increased Cx43 expression, which is associated to TJs and AJs decreased protein expression, such as ZO-1, claudin, and vascular endothelial (VE)-cadherin, respectively, or increased Cx43 GJ channels improving the spread of signaling molecules or ions such as IP3 and Ca2+, which affects vascular hyperpermeability [152,153,154,161,183,184,185].