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The role of CD38 in ischemia reperfusion injury in cardiopulmonary bypass and thoracic transplantation: a narrative review

BACKGROUND AND OBJECTIVE: Ischemia reperfusion injury (IRI) is often the underlying cause of endothelium breakdown and damage in cardiac or transplantation operations, which can lead to disastrous post-operative consequences. Recent studies of cluster of differentiation 38 (CD38) have identified its...

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Autores principales: Gouchoe, Doug A., Vijayakumar, Ammu, Aly, Ahmed H., Cui, Ervin Y., Essandoh, Michael, Gumina, Richard J., Black, Sylvester M., Whitson, Bryan A.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: AME Publishing Company 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10636473/
https://www.ncbi.nlm.nih.gov/pubmed/37969313
http://dx.doi.org/10.21037/jtd-23-725
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author Gouchoe, Doug A.
Vijayakumar, Ammu
Aly, Ahmed H.
Cui, Ervin Y.
Essandoh, Michael
Gumina, Richard J.
Black, Sylvester M.
Whitson, Bryan A.
author_facet Gouchoe, Doug A.
Vijayakumar, Ammu
Aly, Ahmed H.
Cui, Ervin Y.
Essandoh, Michael
Gumina, Richard J.
Black, Sylvester M.
Whitson, Bryan A.
author_sort Gouchoe, Doug A.
collection PubMed
description BACKGROUND AND OBJECTIVE: Ischemia reperfusion injury (IRI) is often the underlying cause of endothelium breakdown and damage in cardiac or transplantation operations, which can lead to disastrous post-operative consequences. Recent studies of cluster of differentiation 38 (CD38) have identified its critical role in IRI. Our objective is to provide a comprehensive overview of CD38-mediated axis, pathways, and potential CD38 translational therapies for reducing inflammation associated with cardiopulmonary bypass (CPB) or thoracic transplantation and IRI. METHODS: We conducted a review of the literature by performing a search of the PubMed database on 2 April 2023. To find relevant publications on CD38, we utilized the MeSH terms: “CD38” AND “Ischemia” OR “CD38” AND “Transplant” OR “CD38” AND “Heart” from 1990–2023. Additional papers were included if they were felt to be relevant but were not captured in the MeSH terms. We found 160 papers that met this criterion, and following screening, exclusion and consensus a total of 36 papers were included. KEY CONTENT AND FINDINGS: CD38 is most notably a nicotine adenine dinucleotide (NAD)(+) glycohydrolase (NADase), and a generator of Ca(2+) signaling secondary messengers. Ultimately, the release of these secondary messengers leads to the activation of important mediators of cellular death. In the heart and during thoracic transplantation, this pathway is intimately involved in a wide variety of injuries; namely the endothelium. In the heart, activation generally results in vasoconstriction, poor myocardial perfusion, and ultimately poor cardiac function. CD38 activation also prevents the accumulation of atherosclerotic disease. During transplantation, intracellular activation leads to infiltration of recipient innate immune cells, tissue edema, and ultimately primary graft dysfunction (PGD). Specifically, in heart transplantation, extracellular activation could be protective and improve allograft survival. CONCLUSIONS: The knowledge gap in understanding the molecular basis of IRI has prevented further development of novel therapies and treatments. The possible interaction of CD38 with CD39 in the endothelium, and the modulation of the CD38 axis may be a pathway to improve cardiovascular outcomes, heart and lung donor organ quality, and overall longevity.
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spelling pubmed-106364732023-11-15 The role of CD38 in ischemia reperfusion injury in cardiopulmonary bypass and thoracic transplantation: a narrative review Gouchoe, Doug A. Vijayakumar, Ammu Aly, Ahmed H. Cui, Ervin Y. Essandoh, Michael Gumina, Richard J. Black, Sylvester M. Whitson, Bryan A. J Thorac Dis Review Article BACKGROUND AND OBJECTIVE: Ischemia reperfusion injury (IRI) is often the underlying cause of endothelium breakdown and damage in cardiac or transplantation operations, which can lead to disastrous post-operative consequences. Recent studies of cluster of differentiation 38 (CD38) have identified its critical role in IRI. Our objective is to provide a comprehensive overview of CD38-mediated axis, pathways, and potential CD38 translational therapies for reducing inflammation associated with cardiopulmonary bypass (CPB) or thoracic transplantation and IRI. METHODS: We conducted a review of the literature by performing a search of the PubMed database on 2 April 2023. To find relevant publications on CD38, we utilized the MeSH terms: “CD38” AND “Ischemia” OR “CD38” AND “Transplant” OR “CD38” AND “Heart” from 1990–2023. Additional papers were included if they were felt to be relevant but were not captured in the MeSH terms. We found 160 papers that met this criterion, and following screening, exclusion and consensus a total of 36 papers were included. KEY CONTENT AND FINDINGS: CD38 is most notably a nicotine adenine dinucleotide (NAD)(+) glycohydrolase (NADase), and a generator of Ca(2+) signaling secondary messengers. Ultimately, the release of these secondary messengers leads to the activation of important mediators of cellular death. In the heart and during thoracic transplantation, this pathway is intimately involved in a wide variety of injuries; namely the endothelium. In the heart, activation generally results in vasoconstriction, poor myocardial perfusion, and ultimately poor cardiac function. CD38 activation also prevents the accumulation of atherosclerotic disease. During transplantation, intracellular activation leads to infiltration of recipient innate immune cells, tissue edema, and ultimately primary graft dysfunction (PGD). Specifically, in heart transplantation, extracellular activation could be protective and improve allograft survival. CONCLUSIONS: The knowledge gap in understanding the molecular basis of IRI has prevented further development of novel therapies and treatments. The possible interaction of CD38 with CD39 in the endothelium, and the modulation of the CD38 axis may be a pathway to improve cardiovascular outcomes, heart and lung donor organ quality, and overall longevity. AME Publishing Company 2023-09-11 2023-10-31 /pmc/articles/PMC10636473/ /pubmed/37969313 http://dx.doi.org/10.21037/jtd-23-725 Text en 2023 Journal of Thoracic Disease. All rights reserved. https://creativecommons.org/licenses/by-nc-nd/4.0/Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0 (https://creativecommons.org/licenses/by-nc-nd/4.0/) .
spellingShingle Review Article
Gouchoe, Doug A.
Vijayakumar, Ammu
Aly, Ahmed H.
Cui, Ervin Y.
Essandoh, Michael
Gumina, Richard J.
Black, Sylvester M.
Whitson, Bryan A.
The role of CD38 in ischemia reperfusion injury in cardiopulmonary bypass and thoracic transplantation: a narrative review
title The role of CD38 in ischemia reperfusion injury in cardiopulmonary bypass and thoracic transplantation: a narrative review
title_full The role of CD38 in ischemia reperfusion injury in cardiopulmonary bypass and thoracic transplantation: a narrative review
title_fullStr The role of CD38 in ischemia reperfusion injury in cardiopulmonary bypass and thoracic transplantation: a narrative review
title_full_unstemmed The role of CD38 in ischemia reperfusion injury in cardiopulmonary bypass and thoracic transplantation: a narrative review
title_short The role of CD38 in ischemia reperfusion injury in cardiopulmonary bypass and thoracic transplantation: a narrative review
title_sort role of cd38 in ischemia reperfusion injury in cardiopulmonary bypass and thoracic transplantation: a narrative review
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10636473/
https://www.ncbi.nlm.nih.gov/pubmed/37969313
http://dx.doi.org/10.21037/jtd-23-725
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