Next Article in Journal
Characterization of In Vivo Function(s) of Members of the Plant Mitochondrial Carrier Family
Next Article in Special Issue
Antagonistic Functions of Connexin 43 during the Development of Primary or Secondary Bone Tumors
Previous Article in Journal
Multiple Screening of Pesticides Toxicity in Zebrafish and Daphnia Based on Locomotor Activity Alterations
Previous Article in Special Issue
Connexin-46 Contained in Extracellular Vesicles Enhance Malignancy Features in Breast Cancer Cells

Canonical and Non-Canonical Roles of Connexin43 in Cardioprotection

Department of Pathology and Immunology, University of Geneva, CH-1211 Geneva, Switzerland
Univ Coimbra, Institute for Clinical and Biomedical Research (iCBR), Faculty of Medicine, 3000-548 Coimbra, Portugal
Univ Coimbra, Center for Innovative Biomedicine and Biotechnology (CIBB), 3000-548 Coimbra, Portugal
Clinical Academic Centre of Coimbra (CACC), 3000-548 Coimbra, Portugal
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;
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
Show Figures

Figure 1

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.

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.

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.

Find Other Styles
Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Article Access Map by Country/Region

Back to TopTop