Nicotinamide adenine dinucleotide: Biosynthesis, consumption and therapeutic role in cardiac diseases.
Identifieur interne : 000A57 ( Main/Exploration ); précédent : 000A56; suivant : 000A58Nicotinamide adenine dinucleotide: Biosynthesis, consumption and therapeutic role in cardiac diseases.
Auteurs : Cynthia Tannous [Liban] ; George W. Booz [États-Unis] ; Raffaele Altara [États-Unis, Norvège] ; Dina H. Muhieddine [Liban] ; Mathias Mericskay [France] ; Marwan M. Refaat [Liban] ; Fouad A. Zouein [Liban]Source :
- Acta physiologica (Oxford, England) [ 1748-1716 ] ; 2020.
Abstract
Nicotinamide adenine dinucleotide (NAD) is an abundant cofactor that plays crucial roles in several cellular processes. NAD can be synthesized de novo starting with tryptophan, or from salvage pathways starting with NAD precursors like nicotinic acid (NA), nicotinamide (NAM) or nicotinamide riboside (NR), referred to as niacin/B3 vitamins, arising from dietary supply or from cellular NAD catabolism. Given the interconversion between its oxidized (NAD+ ) and reduced form (NADH), NAD participates in a wide range of reactions: regulation of cellular redox status, energy metabolism and mitochondrial biogenesis. Plus, NAD acts as a signalling molecule, being a cosubstrate for several enzymes such as sirtuins, poly-ADP-ribose-polymerases (PARPs) and some ectoenzymes like CD38, regulating critical biological processes like gene expression, DNA repair, calcium signalling and circadian rhythms. Given the large number of mitochondria present in cardiac tissue, the heart has the highest NAD levels and is one of the most metabolically demanding organs. In several models of heart failure, myocardial NAD levels are depressed and this depression is caused by mitochondrial dysfunction, metabolic remodelling and inflammation. Emerging evidence suggests that regulating NAD homeostasis by NAD precursor supplementation has therapeutic efficiency in improving myocardial bioenergetics and function. This review provides an overview of the latest understanding of the different NAD biosynthesis pathways, as well as its role as a signalling molecule particularly in cardiac tissue. We highlight the significance of preserving NAD equilibrium in various models of heart diseases and shed light on the potential pharmacological interventions aiming to use NAD boosters as therapeutic agents.
DOI: 10.1111/apha.13551
PubMed: 32853469
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Zouein</name><affiliation wicri:level="1"><nlm:affiliation>Department of Pharmacology and Toxicology, Faculty of Medicine, American University of Beirut Medical Center, Beirut, Lebanon.</nlm:affiliation><country xml:lang="fr">Liban</country><wicri:regionArea>Department of Pharmacology and Toxicology, Faculty of Medicine, American University of Beirut Medical Center, Beirut</wicri:regionArea><wicri:noRegion>Beirut</wicri:noRegion></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2020">2020</date><idno type="RBID">pubmed:32853469</idno><idno type="pmid">32853469</idno><idno type="doi">10.1111/apha.13551</idno><idno type="wicri:Area/Main/Corpus">000340</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Corpus" wicri:corpus="PubMed">000340</idno><idno type="wicri:Area/Main/Curation">000340</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Curation">000340</idno><idno type="wicri:Area/Main/Exploration">000340</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Nicotinamide adenine dinucleotide: Biosynthesis, consumption and therapeutic role in cardiac diseases.</title><author><name sortKey="Tannous, Cynthia" sort="Tannous, Cynthia" uniqKey="Tannous C" first="Cynthia" last="Tannous">Cynthia Tannous</name><affiliation wicri:level="1"><nlm:affiliation>Department of Pharmacology and Toxicology, Faculty of Medicine, American University of Beirut Medical Center, Beirut, Lebanon.</nlm:affiliation><country xml:lang="fr">Liban</country><wicri:regionArea>Department of Pharmacology and Toxicology, Faculty of Medicine, American University of Beirut Medical Center, Beirut</wicri:regionArea><wicri:noRegion>Beirut</wicri:noRegion></affiliation></author><author><name sortKey="Booz, George W" sort="Booz, George W" uniqKey="Booz G" first="George W" last="Booz">George W. Booz</name><affiliation wicri:level="2"><nlm:affiliation>Department of Pharmacology and Toxicology, University of Mississippi Medical Center, Jackson, MS, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Pharmacology and Toxicology, University of Mississippi Medical Center, Jackson, MS</wicri:regionArea><placeName><region type="state">État du Mississippi</region></placeName></affiliation></author><author><name sortKey="Altara, Raffaele" sort="Altara, Raffaele" uniqKey="Altara R" first="Raffaele" last="Altara">Raffaele Altara</name><affiliation wicri:level="2"><nlm:affiliation>Department of Pathology, School of Medicine, University of Mississippi Medical Center, Jackson, MS, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Pathology, School of Medicine, University of Mississippi Medical Center, Jackson, MS</wicri:regionArea><placeName><region type="state">État du Mississippi</region></placeName></affiliation><affiliation wicri:level="3"><nlm:affiliation>Institute for Experimental Medical Research, Oslo University Hospital and University of Oslo, Oslo, Norway.</nlm:affiliation><country xml:lang="fr">Norvège</country><wicri:regionArea>Institute for Experimental Medical Research, Oslo University Hospital and University of Oslo, Oslo</wicri:regionArea><placeName><settlement type="city">Oslo</settlement><region nuts="2">Østlandet</region></placeName></affiliation><affiliation wicri:level="3"><nlm:affiliation>KG Jebsen Center for Cardiac Research, University of Oslo, Oslo, Norway.</nlm:affiliation><country xml:lang="fr">Norvège</country><wicri:regionArea>KG Jebsen Center for Cardiac Research, University of Oslo, Oslo</wicri:regionArea><placeName><settlement type="city">Oslo</settlement><region nuts="2">Østlandet</region></placeName></affiliation></author><author><name sortKey="Muhieddine, Dina H" sort="Muhieddine, Dina H" uniqKey="Muhieddine D" first="Dina H" last="Muhieddine">Dina H. Muhieddine</name><affiliation wicri:level="1"><nlm:affiliation>Department of Pharmacology and Toxicology, Faculty of Medicine, American University of Beirut Medical Center, Beirut, Lebanon.</nlm:affiliation><country xml:lang="fr">Liban</country><wicri:regionArea>Department of Pharmacology and Toxicology, Faculty of Medicine, American University of Beirut Medical Center, Beirut</wicri:regionArea><wicri:noRegion>Beirut</wicri:noRegion></affiliation></author><author><name sortKey="Mericskay, Mathias" sort="Mericskay, Mathias" uniqKey="Mericskay M" first="Mathias" last="Mericskay">Mathias Mericskay</name><affiliation wicri:level="1"><nlm:affiliation>INSERM Department of Signalling and Cardiovascular Pathophysiology, UMR-S 1180, Université Paris-Saclay, Châtenay-Malabry, France.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>INSERM Department of Signalling and Cardiovascular Pathophysiology, UMR-S 1180, Université Paris-Saclay, Châtenay-Malabry</wicri:regionArea><wicri:noRegion>Châtenay-Malabry</wicri:noRegion><wicri:noRegion>Châtenay-Malabry</wicri:noRegion></affiliation></author><author><name sortKey="Refaat, Marwan M" sort="Refaat, Marwan M" uniqKey="Refaat M" first="Marwan M" last="Refaat">Marwan M. Refaat</name><affiliation wicri:level="1"><nlm:affiliation>Department of Internal Medicine, Faculty of Medicine, American University of Beirut Medical Center, Beirut, Lebanon.</nlm:affiliation><country xml:lang="fr">Liban</country><wicri:regionArea>Department of Internal Medicine, Faculty of Medicine, American University of Beirut Medical Center, Beirut</wicri:regionArea><wicri:noRegion>Beirut</wicri:noRegion></affiliation><affiliation wicri:level="1"><nlm:affiliation>Department of Biochemistry and Molecular Genetics, Faculty of Medicine, American University of Beirut Medical Center, Beirut, Lebanon.</nlm:affiliation><country xml:lang="fr">Liban</country><wicri:regionArea>Department of Biochemistry and Molecular Genetics, Faculty of Medicine, American University of Beirut Medical Center, Beirut</wicri:regionArea><wicri:noRegion>Beirut</wicri:noRegion></affiliation></author><author><name sortKey="Zouein, Fouad A" sort="Zouein, Fouad A" uniqKey="Zouein F" first="Fouad A" last="Zouein">Fouad A. Zouein</name><affiliation wicri:level="1"><nlm:affiliation>Department of Pharmacology and Toxicology, Faculty of Medicine, American University of Beirut Medical Center, Beirut, Lebanon.</nlm:affiliation><country xml:lang="fr">Liban</country><wicri:regionArea>Department of Pharmacology and Toxicology, Faculty of Medicine, American University of Beirut Medical Center, Beirut</wicri:regionArea><wicri:noRegion>Beirut</wicri:noRegion></affiliation></author></analytic><series><title level="j">Acta physiologica (Oxford, England)</title><idno type="eISSN">1748-1716</idno><imprint><date when="2020" type="published">2020</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Nicotinamide adenine dinucleotide (NAD) is an abundant cofactor that plays crucial roles in several cellular processes. NAD can be synthesized de novo starting with tryptophan, or from salvage pathways starting with NAD precursors like nicotinic acid (NA), nicotinamide (NAM) or nicotinamide riboside (NR), referred to as niacin/B<sub>3</sub> vitamins, arising from dietary supply or from cellular NAD catabolism. Given the interconversion between its oxidized (NAD<sup>+</sup> ) and reduced form (NADH), NAD participates in a wide range of reactions: regulation of cellular redox status, energy metabolism and mitochondrial biogenesis. Plus, NAD acts as a signalling molecule, being a cosubstrate for several enzymes such as sirtuins, poly-ADP-ribose-polymerases (PARPs) and some ectoenzymes like CD38, regulating critical biological processes like gene expression, DNA repair, calcium signalling and circadian rhythms. Given the large number of mitochondria present in cardiac tissue, the heart has the highest NAD levels and is one of the most metabolically demanding organs. In several models of heart failure, myocardial NAD levels are depressed and this depression is caused by mitochondrial dysfunction, metabolic remodelling and inflammation. Emerging evidence suggests that regulating NAD homeostasis by NAD precursor supplementation has therapeutic efficiency in improving myocardial bioenergetics and function. This review provides an overview of the latest understanding of the different NAD biosynthesis pathways, as well as its role as a signalling molecule particularly in cardiac tissue. We highlight the significance of preserving NAD equilibrium in various models of heart diseases and shed light on the potential pharmacological interventions aiming to use NAD boosters as therapeutic agents.</div></front></TEI><pubmed><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">32853469</PMID><DateRevised><Year>2020</Year><Month>09</Month><Day>22</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1748-1716</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2020</Year><Month>Aug</Month><Day>27</Day></PubDate></JournalIssue><Title>Acta physiologica (Oxford, England)</Title><ISOAbbreviation>Acta Physiol (Oxf)</ISOAbbreviation></Journal><ArticleTitle>Nicotinamide adenine dinucleotide: Biosynthesis, consumption and therapeutic role in cardiac diseases.</ArticleTitle><Pagination><MedlinePgn>e13551</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1111/apha.13551</ELocationID><Abstract><AbstractText>Nicotinamide adenine dinucleotide (NAD) is an abundant cofactor that plays crucial roles in several cellular processes. NAD can be synthesized de novo starting with tryptophan, or from salvage pathways starting with NAD precursors like nicotinic acid (NA), nicotinamide (NAM) or nicotinamide riboside (NR), referred to as niacin/B<sub>3</sub> vitamins, arising from dietary supply or from cellular NAD catabolism. Given the interconversion between its oxidized (NAD<sup>+</sup> ) and reduced form (NADH), NAD participates in a wide range of reactions: regulation of cellular redox status, energy metabolism and mitochondrial biogenesis. Plus, NAD acts as a signalling molecule, being a cosubstrate for several enzymes such as sirtuins, poly-ADP-ribose-polymerases (PARPs) and some ectoenzymes like CD38, regulating critical biological processes like gene expression, DNA repair, calcium signalling and circadian rhythms. Given the large number of mitochondria present in cardiac tissue, the heart has the highest NAD levels and is one of the most metabolically demanding organs. In several models of heart failure, myocardial NAD levels are depressed and this depression is caused by mitochondrial dysfunction, metabolic remodelling and inflammation. Emerging evidence suggests that regulating NAD homeostasis by NAD precursor supplementation has therapeutic efficiency in improving myocardial bioenergetics and function. This review provides an overview of the latest understanding of the different NAD biosynthesis pathways, as well as its role as a signalling molecule particularly in cardiac tissue. We highlight the significance of preserving NAD equilibrium in various models of heart diseases and shed light on the potential pharmacological interventions aiming to use NAD boosters as therapeutic agents.</AbstractText><CopyrightInformation>© 2020 Scandinavian Physiological Society. Published by John Wiley & Sons Ltd.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Tannous</LastName><ForeName>Cynthia</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Department of Pharmacology and Toxicology, Faculty of Medicine, American University of Beirut Medical Center, Beirut, Lebanon.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Booz</LastName><ForeName>George W</ForeName><Initials>GW</Initials><AffiliationInfo><Affiliation>Department of Pharmacology and Toxicology, University of Mississippi Medical Center, Jackson, MS, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Altara</LastName><ForeName>Raffaele</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Department of Pathology, School of Medicine, University of Mississippi Medical Center, Jackson, MS, USA.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Institute for Experimental Medical Research, Oslo University Hospital and University of Oslo, Oslo, Norway.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>KG Jebsen Center for Cardiac Research, University of Oslo, Oslo, Norway.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Muhieddine</LastName><ForeName>Dina H</ForeName><Initials>DH</Initials><AffiliationInfo><Affiliation>Department of Pharmacology and Toxicology, Faculty of Medicine, American University of Beirut Medical Center, Beirut, Lebanon.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Mericskay</LastName><ForeName>Mathias</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>INSERM Department of Signalling and Cardiovascular Pathophysiology, UMR-S 1180, Université Paris-Saclay, Châtenay-Malabry, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Refaat</LastName><ForeName>Marwan M</ForeName><Initials>MM</Initials><AffiliationInfo><Affiliation>Department of Internal Medicine, Faculty of Medicine, American University of Beirut Medical Center, Beirut, Lebanon.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Biochemistry and Molecular Genetics, Faculty of Medicine, American University of Beirut Medical Center, Beirut, Lebanon.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zouein</LastName><ForeName>Fouad A</ForeName><Initials>FA</Initials><Identifier Source="ORCID">https://orcid.org/0000-0003-4451-804X</Identifier><AffiliationInfo><Affiliation>Department of Pharmacology and Toxicology, Faculty of Medicine, American University of Beirut Medical Center, Beirut, Lebanon.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>CNRS-103487</GrantID><Agency>Centre National de la Recherche Scientifique</Agency><Country></Country></Grant><Grant><GrantID>CNRS-103507</GrantID><Agency>Centre National de la Recherche Scientifique</Agency><Country></Country></Grant><Grant><GrantID>MPP-320095</GrantID><Agency>AUBMC Medical Practice Plan</Agency><Country></Country></Grant><Grant><GrantID>MPP320145</GrantID><Agency>AUBMC Medical Practice Plan</Agency><Country></Country></Grant><Grant><GrantID>0075811</GrantID><Agency>Fondation de France</Agency><Country></Country></Grant><Grant><GrantID>100410</GrantID><Agency>AUMBC - Seed Grant</Agency><Country></Country></Grant><Grant><GrantID>CRS-103556</GrantID><Agency>AUBMC - Collaborative Research Stimulus</Agency><Country></Country></Grant><Grant><GrantID>ANR-17-CE17-0015-01</GrantID><Agency>Agence Nationale pour la Recherche</Agency><Country></Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2020</Year><Month>08</Month><Day>27</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Acta Physiol (Oxf)</MedlineTA><NlmUniqueID>101262545</NlmUniqueID><ISSNLinking>1748-1708</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">COVID-19</Keyword><Keyword MajorTopicYN="N">NAD</Keyword><Keyword MajorTopicYN="N">cardiac diseases</Keyword><Keyword MajorTopicYN="N">cardiac metabolism</Keyword><Keyword MajorTopicYN="N">inflammation</Keyword><Keyword MajorTopicYN="N">mitochondria</Keyword><Keyword MajorTopicYN="N">redox potential</Keyword><Keyword MajorTopicYN="N">transcription factors</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2020</Year><Month>06</Month><Day>24</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2020</Year><Month>08</Month><Day>05</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2020</Year><Month>08</Month><Day>07</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2020</Year><Month>8</Month><Day>28</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2020</Year><Month>8</Month><Day>28</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2020</Year><Month>8</Month><Day>28</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>aheadofprint</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">32853469</ArticleId><ArticleId IdType="doi">10.1111/apha.13551</ArticleId></ArticleIdList><ReferenceList><Title>REFERENCES</Title><Reference><Citation>Young AHaWJ. 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Refaat</name><name sortKey="Refaat, Marwan M" sort="Refaat, Marwan M" uniqKey="Refaat M" first="Marwan M" last="Refaat">Marwan M. Refaat</name><name sortKey="Zouein, Fouad A" sort="Zouein, Fouad A" uniqKey="Zouein F" first="Fouad A" last="Zouein">Fouad A. Zouein</name></country><country name="États-Unis"><region name="État du Mississippi"><name sortKey="Booz, George W" sort="Booz, George W" uniqKey="Booz G" first="George W" last="Booz">George W. Booz</name></region><name sortKey="Altara, Raffaele" sort="Altara, Raffaele" uniqKey="Altara R" first="Raffaele" last="Altara">Raffaele Altara</name></country><country name="Norvège"><region name="Østlandet"><name sortKey="Altara, Raffaele" sort="Altara, Raffaele" uniqKey="Altara R" first="Raffaele" last="Altara">Raffaele Altara</name></region><name sortKey="Altara, Raffaele" sort="Altara, Raffaele" uniqKey="Altara R" first="Raffaele" last="Altara">Raffaele Altara</name></country><country name="France"><noRegion><name sortKey="Mericskay, Mathias" sort="Mericskay, Mathias" uniqKey="Mericskay M" first="Mathias" last="Mericskay">Mathias Mericskay</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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