Background　Connexin43（Cx43） is the major protein of gap junction in the heart. A series of cardiac pathologic processes， such as heart failure and arrhythmias， facilitate Cx43 redistribution to the lateral membrane of the cardiomyocytes from the intercalated disc. The occurrence of gap junctions uncoupling after Cx43 lateralization can lead to reentrant arrhythmias and cardiac dysfunction.　Objective　To elaborate the molecular mechanisms of myocardial Cx43 lateralization through the process of Cx43 transportation and location.　Content　The lateralization of Cx43 was proposed to be closely associated with the loss of coupling with connexins（Cxs）， i.e.， N-cadherin， desmosomes， Zonula Occludens-1（ZO-1）， and cytoskeletal proteins-mediated forward trafficking of Cx43. Moreover， phosphorylation or acetylation of Cx43 was also involved in its lateralization. This review focusess on the Cxs， cytoskeletal proteins， phosphorylation， and acetylation of Cx43 to show the probable molecular mechanisms of Cx43 lateralization.　Trend　To provide new ideas and molecular mechanisms for further research into the mechanisms of Cx43 lateralization and the therapy of reentrant arrhythmias.