Rusiecka OM Montgomery J Morel S Batista-Almeida D Van Campenhout R Vinken M Girao H Kwak BR 2020 Since the mid-20th century, ischemic heart disease has been the world's leading cause of death. Developing effective clinical cardioprotection strategies would make a significant impact in improving both quality of life and longevity in the worldwide population. Both ex vivo and in vivo animal models of cardiac ischemia/reperfusion (I/R) injury are robustly used in research. Connexin43 (Cx43), the predominant gap junction channel-forming protein in cardiomyocytes, has emerged as a cardioprotective target. Cx43 posttranslational modifications as well as cellular distribution are altered during cardiac reperfusion injury, inducing phosphorylation states and localization detrimental to maintaining intercellular communication and cardiac conduction. Pre- (before ischemia) and post- (after ischemia but before reperfusion) conditioning can abrogate this injury process, preserving Cx43 and reducing cell death. Pre-/post-conditioning has been shown to largely rely on the presence of Cx43, including mitochondrial Cx43, which is implicated to play a major role in pre-conditioning. Posttranslational modifications of Cx43 after injury alter the protein interactome, inducing negative protein cascades and altering protein trafficking, which then causes further damage post-I/R injury. Recently, several peptides based on the Cx43 sequence have been found to successfully diminish cardiac injury in pre-clinical studies. application/pdf https://sonar.ch/global/documents/100570 eng info:eu-repo/semantics/altIdentifier/doi/10.3390/biom10091225 info:eu-repo/semantics/altIdentifier/pmid/32842488 info:eu-repo/semantics/openAccess Biomolecules. - 2020 Cx43 cardioprotection connexin gap junction hemi-channel ischemia/reperfusion injury myocardial infarction Canonical and Non-Canonical Roles of Connexin43 in Cardioprotection. http://purl.org/coar/resource_type/c_6501