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Canonical and Non-Canonical Roles of Connexin43 in Cardioprotection

1
Department of Pathology and Immunology, University of Geneva, CH-1211 Geneva, Switzerland
2
Univ Coimbra, Institute for Clinical and Biomedical Research (iCBR), Faculty of Medicine, 3000-548 Coimbra, Portugal
3
Univ Coimbra, Center for Innovative Biomedicine and Biotechnology (CIBB), 3000-548 Coimbra, Portugal
4
Clinical Academic Centre of Coimbra (CACC), 3000-548 Coimbra, Portugal
5
Department of In Vitro Toxicology and Dermato-Cosmetology, Vrije Universiteit Brussel, 1090 Brussels, Belgium
*
Author to whom correspondence should be addressed.
Equal contribution of authors.
Biomolecules 2020, 10(9), 1225; https://doi.org/10.3390/biom10091225
Received: 27 July 2020 / Revised: 17 August 2020 / Accepted: 20 August 2020 / Published: 23 August 2020
(This article belongs to the Special Issue Connexins, Innexins, and Pannexins: From Biology to Clinical Targets)
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. View Full-Text
Keywords: connexin; Cx43; gap junction; hemi-channel; cardioprotection; myocardial infarction; ischemia/reperfusion injury connexin; Cx43; gap junction; hemi-channel; cardioprotection; myocardial infarction; ischemia/reperfusion injury
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MDPI and ACS Style

Rusiecka, O.M.; Montgomery, J.; Morel, S.; Batista-Almeida, D.; Van Campenhout, R.; Vinken, M.; Girao, H.; Kwak, B.R. Canonical and Non-Canonical Roles of Connexin43 in Cardioprotection. Biomolecules 2020, 10, 1225. https://doi.org/10.3390/biom10091225

AMA Style

Rusiecka OM, Montgomery J, Morel S, Batista-Almeida D, Van Campenhout R, Vinken M, Girao H, Kwak BR. Canonical and Non-Canonical Roles of Connexin43 in Cardioprotection. Biomolecules. 2020; 10(9):1225. https://doi.org/10.3390/biom10091225

Chicago/Turabian Style

Rusiecka, Olga M., Jade Montgomery, Sandrine Morel, Daniela Batista-Almeida, Raf Van Campenhout, Mathieu Vinken, Henrique Girao, and Brenda R. Kwak. 2020. "Canonical and Non-Canonical Roles of Connexin43 in Cardioprotection" Biomolecules 10, no. 9: 1225. https://doi.org/10.3390/biom10091225

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