DetoxFungiV1, Main, Exploration, bibRecord, 000494

Glyoxalase 1 Prevents Chronic Hyperglycemia Induced Heart-Explant Derived Cell Dysfunction.

Identifieur interne : 000494 ( Main/Exploration ); précédent : 000493; suivant : 000495

Glyoxalase 1 Prevents Chronic Hyperglycemia Induced Heart-Explant Derived Cell Dysfunction.

Auteurs : Melanie Villanueva [Canada] ; Connor Michie [Canada] ; Sandrine Parent [Canada] ; Georges N. Kanaan [Canada] ; Ghazaleh Rafatian [Canada] ; Pushpinder Kanda [Canada] ; Bin Ye [Canada] ; Wenbin Liang [Canada] ; Mary-Ellen Harper [Canada] ; Darryl R. Davis [Canada]

Source :

Theranostics [ 1838-7640 ] ; 2019.

RBID : pubmed:31534514

Descripteurs français

KwdFr :
- Animaux (MeSH), Antioxydants (métabolisme), Complications du diabète (MeSH), Défaillance cardiaque (enzymologie), Défaillance cardiaque (prévention et contrôle), Espèces réactives de l'oxygène (métabolisme), Humains (MeSH), Hyperglycémie (complications), Infarctus du myocarde (enzymologie), Infarctus du myocarde (prévention et contrôle), Infarctus du myocarde (étiologie), Lactoyl glutathione lyase (génétique), Lactoyl glutathione lyase (métabolisme), Maladie chronique (MeSH), Souris (MeSH), Souris de lignée C57BL (MeSH), Souris transgéniques (MeSH), Stress oxydatif (MeSH), Thérapie cellulaire et tissulaire (MeSH), Vésicules extracellulaires (métabolisme).
MESH :
- enzymologie : Défaillance cardiaque, Infarctus du myocarde.
- génétique : Hyperglycémie, Lactoyl glutathione lyase.
- métabolisme : Antioxydants, Espèces réactives de l'oxygène, Lactoyl glutathione lyase, Vésicules extracellulaires.
- prévention et contrôle : Défaillance cardiaque, Infarctus du myocarde.
- étiologie : Infarctus du myocarde.
- Animaux, Complications du diabète, Humains, Maladie chronique, Souris, Souris de lignée C57BL, Souris transgéniques, Stress oxydatif, Thérapie cellulaire et tissulaire.

English descriptors

KwdEn :
- Animals (MeSH), Antioxidants (metabolism), Cell- and Tissue-Based Therapy (MeSH), Chronic Disease (MeSH), Diabetes Complications (MeSH), Extracellular Vesicles (metabolism), Heart Failure (enzymology), Heart Failure (prevention & control), Humans (MeSH), Hyperglycemia (complications), Lactoylglutathione Lyase (genetics), Lactoylglutathione Lyase (metabolism), Mice (MeSH), Mice, Inbred C57BL (MeSH), Mice, Transgenic (MeSH), Myocardial Infarction (enzymology), Myocardial Infarction (etiology), Myocardial Infarction (prevention & control), Oxidative Stress (MeSH), Reactive Oxygen Species (metabolism).
MESH :
- chemical , genetics : Lactoylglutathione Lyase.
- chemical , metabolism : Antioxidants, Lactoylglutathione Lyase, Reactive Oxygen Species.
- complications : Hyperglycemia.
- enzymology : Heart Failure, Myocardial Infarction.
- etiology : Myocardial Infarction.
- metabolism : Extracellular Vesicles.
- prevention & control : Heart Failure, Myocardial Infarction.
- Animals, Cell- and Tissue-Based Therapy, Chronic Disease, Diabetes Complications, Humans, Mice, Mice, Inbred C57BL, Mice, Transgenic, Oxidative Stress.

Abstract

Decades of work have shown that diabetes increases the risk of heart disease and worsens clinical outcomes after myocardial infarction. Because diabetes is an absolute contraindication to heart transplant, cell therapy is increasingly being explored as a means of improving heart function for these patients with very few other options. Given that hyperglycemia promotes the generation of toxic metabolites, the influence of the key detoxification enzyme glyoxalase 1 (Glo1) on chronic hyperglycemia induced heart explant-derived cell (EDC) dysfunction was investigated. Methods: EDCs were cultured from wild type C57Bl/6 or Glo1 over-expressing transgenic mice 2 months after treatment with the pancreatic beta cell toxin streptozotocin or vehicle. The effects of Glo1 overexpression was evaluated using in vitro and in vivo models of myocardial ischemia. Results: Chronic hyperglycemia reduced overall culture yields and increased the reactive dicarbonyl cell burden within EDCs. These intrinsic cell changes reduced the angiogenic potential and production of pro-healing exosomes while promoting senescence and slowing proliferation. Compared to intra-myocardial injection of normoglycemic cells, chronic hyperglycemia attenuated cell-mediated improvements in myocardial function and reduced the ability of transplanted cells to promote new blood vessel and cardiomyocyte growth. In contrast, Glo1 overexpression decreased oxidative damage while restoring both cell culture yields and EDC-mediated repair of ischemic myocardium. The latter was associated with enhanced production of pro-healing extracellular vesicles by Glo1 cells without altering the pro-healing microRNA cargo within. Conclusions: Chronic hyperglycemia decreases the regenerative performance of EDCs. Overexpression of Glo1 reduces dicarbonyl stress and prevents chronic hyperglycemia-induced dysfunction by rejuvenating the production of pro-healing extracellular vesicles.

DOI: 10.7150/thno.36639
PubMed: 31534514
PubMed Central: PMC6735395

Affiliations:

Links toward previous steps (curation, corpus...)

to stream Main, to step Corpus: 000338
to stream Main, to step Curation: 000338

Le document en format XML

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<sourceDesc><biblStruct><analytic><title xml:lang="en">Glyoxalase 1 Prevents Chronic Hyperglycemia Induced Heart-Explant Derived Cell Dysfunction.</title>
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<author><name sortKey="Ye, Bin" sort="Ye, Bin" uniqKey="Ye B" first="Bin" last="Ye">Bin Ye</name>
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<region type="state">Ontario</region>
</placeName>
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<country>Canada</country>
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<region type="state">Ontario</region>
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<author><name sortKey="Harper, Mary Ellen" sort="Harper, Mary Ellen" uniqKey="Harper M" first="Mary-Ellen" last="Harper">Mary-Ellen Harper</name>
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<country>Canada</country>
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<series><title level="j">Theranostics</title>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals (MeSH)</term>
<term>Antioxidants (metabolism)</term>
<term>Cell- and Tissue-Based Therapy (MeSH)</term>
<term>Chronic Disease (MeSH)</term>
<term>Diabetes Complications (MeSH)</term>
<term>Extracellular Vesicles (metabolism)</term>
<term>Heart Failure (enzymology)</term>
<term>Heart Failure (prevention & control)</term>
<term>Humans (MeSH)</term>
<term>Hyperglycemia (complications)</term>
<term>Lactoylglutathione Lyase (genetics)</term>
<term>Lactoylglutathione Lyase (metabolism)</term>
<term>Mice (MeSH)</term>
<term>Mice, Inbred C57BL (MeSH)</term>
<term>Mice, Transgenic (MeSH)</term>
<term>Myocardial Infarction (enzymology)</term>
<term>Myocardial Infarction (etiology)</term>
<term>Myocardial Infarction (prevention & control)</term>
<term>Oxidative Stress (MeSH)</term>
<term>Reactive Oxygen Species (metabolism)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Animaux (MeSH)</term>
<term>Antioxydants (métabolisme)</term>
<term>Complications du diabète (MeSH)</term>
<term>Défaillance cardiaque (enzymologie)</term>
<term>Défaillance cardiaque (prévention et contrôle)</term>
<term>Espèces réactives de l'oxygène (métabolisme)</term>
<term>Humains (MeSH)</term>
<term>Hyperglycémie (complications)</term>
<term>Infarctus du myocarde (enzymologie)</term>
<term>Infarctus du myocarde (prévention et contrôle)</term>
<term>Infarctus du myocarde (étiologie)</term>
<term>Lactoyl glutathione lyase (génétique)</term>
<term>Lactoyl glutathione lyase (métabolisme)</term>
<term>Maladie chronique (MeSH)</term>
<term>Souris (MeSH)</term>
<term>Souris de lignée C57BL (MeSH)</term>
<term>Souris transgéniques (MeSH)</term>
<term>Stress oxydatif (MeSH)</term>
<term>Thérapie cellulaire et tissulaire (MeSH)</term>
<term>Vésicules extracellulaires (métabolisme)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Lactoylglutathione Lyase</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Antioxidants</term>
<term>Lactoylglutathione Lyase</term>
<term>Reactive Oxygen Species</term>
</keywords>
<keywords scheme="MESH" qualifier="complications" xml:lang="en"><term>Hyperglycemia</term>
</keywords>
<keywords scheme="MESH" qualifier="enzymologie" xml:lang="fr"><term>Défaillance cardiaque</term>
<term>Infarctus du myocarde</term>
</keywords>
<keywords scheme="MESH" qualifier="enzymology" xml:lang="en"><term>Heart Failure</term>
<term>Myocardial Infarction</term>
</keywords>
<keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Myocardial Infarction</term>
</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Hyperglycémie</term>
<term>Lactoyl glutathione lyase</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Extracellular Vesicles</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Antioxydants</term>
<term>Espèces réactives de l'oxygène</term>
<term>Lactoyl glutathione lyase</term>
<term>Vésicules extracellulaires</term>
</keywords>
<keywords scheme="MESH" qualifier="prevention & control" xml:lang="en"><term>Heart Failure</term>
<term>Myocardial Infarction</term>
</keywords>
<keywords scheme="MESH" qualifier="prévention et contrôle" xml:lang="fr"><term>Défaillance cardiaque</term>
<term>Infarctus du myocarde</term>
</keywords>
<keywords scheme="MESH" qualifier="étiologie" xml:lang="fr"><term>Infarctus du myocarde</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Animals</term>
<term>Cell- and Tissue-Based Therapy</term>
<term>Chronic Disease</term>
<term>Diabetes Complications</term>
<term>Humans</term>
<term>Mice</term>
<term>Mice, Inbred C57BL</term>
<term>Mice, Transgenic</term>
<term>Oxidative Stress</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Animaux</term>
<term>Complications du diabète</term>
<term>Humains</term>
<term>Maladie chronique</term>
<term>Souris</term>
<term>Souris de lignée C57BL</term>
<term>Souris transgéniques</term>
<term>Stress oxydatif</term>
<term>Thérapie cellulaire et tissulaire</term>
</keywords>
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<front><div type="abstract" xml:lang="en">Decades of work have shown that diabetes increases the risk of heart disease and worsens clinical outcomes after myocardial infarction. Because diabetes is an absolute contraindication to heart transplant, cell therapy is increasingly being explored as a means of improving heart function for these patients with very few other options. Given that hyperglycemia promotes the generation of toxic metabolites, the influence of the key detoxification enzyme glyoxalase 1 (Glo1) on chronic hyperglycemia induced heart explant-derived cell (EDC) dysfunction was investigated. <b>Methods:</b>
 EDCs were cultured from wild type C57Bl/6 or Glo1 over-expressing transgenic mice 2 months after treatment with the pancreatic beta cell toxin streptozotocin or vehicle. The effects of Glo1 overexpression was evaluated using <i>in vitro</i>
 and <i>in vivo</i>
 models of myocardial ischemia. <b>Results:</b>
 Chronic hyperglycemia reduced overall culture yields and increased the reactive dicarbonyl cell burden within EDCs. These intrinsic cell changes reduced the angiogenic potential and production of pro-healing exosomes while promoting senescence and slowing proliferation. Compared to intra-myocardial injection of normoglycemic cells, chronic hyperglycemia attenuated cell-mediated improvements in myocardial function and reduced the ability of transplanted cells to promote new blood vessel and cardiomyocyte growth. In contrast, Glo1 overexpression decreased oxidative damage while restoring both cell culture yields and EDC-mediated repair of ischemic myocardium. The latter was associated with enhanced production of pro-healing extracellular vesicles by Glo1 cells without altering the pro-healing microRNA cargo within. <b>Conclusions:</b>
 Chronic hyperglycemia decreases the regenerative performance of EDCs. Overexpression of Glo1 reduces dicarbonyl stress and prevents chronic hyperglycemia-induced dysfunction by rejuvenating the production of pro-healing extracellular vesicles.</div>
</front>
</TEI>
<pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">31534514</PMID>
<DateCompleted><Year>2020</Year>
<Month>08</Month>
<Day>18</Day>
</DateCompleted>
<DateRevised><Year>2020</Year>
<Month>08</Month>
<Day>18</Day>
</DateRevised>
<Article PubModel="Electronic-eCollection"><Journal><ISSN IssnType="Electronic">1838-7640</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>9</Volume>
<Issue>19</Issue>
<PubDate><Year>2019</Year>
</PubDate>
</JournalIssue>
<Title>Theranostics</Title>
<ISOAbbreviation>Theranostics</ISOAbbreviation>
</Journal>
<ArticleTitle>Glyoxalase 1 Prevents Chronic Hyperglycemia Induced Heart-Explant Derived Cell Dysfunction.</ArticleTitle>
<Pagination><MedlinePgn>5720-5730</MedlinePgn>
</Pagination>
<ELocationID EIdType="doi" ValidYN="Y">10.7150/thno.36639</ELocationID>
<Abstract><AbstractText>Decades of work have shown that diabetes increases the risk of heart disease and worsens clinical outcomes after myocardial infarction. Because diabetes is an absolute contraindication to heart transplant, cell therapy is increasingly being explored as a means of improving heart function for these patients with very few other options. Given that hyperglycemia promotes the generation of toxic metabolites, the influence of the key detoxification enzyme glyoxalase 1 (Glo1) on chronic hyperglycemia induced heart explant-derived cell (EDC) dysfunction was investigated. <b>Methods:</b>
 EDCs were cultured from wild type C57Bl/6 or Glo1 over-expressing transgenic mice 2 months after treatment with the pancreatic beta cell toxin streptozotocin or vehicle. The effects of Glo1 overexpression was evaluated using <i>in vitro</i>
 and <i>in vivo</i>
 models of myocardial ischemia. <b>Results:</b>
 Chronic hyperglycemia reduced overall culture yields and increased the reactive dicarbonyl cell burden within EDCs. These intrinsic cell changes reduced the angiogenic potential and production of pro-healing exosomes while promoting senescence and slowing proliferation. Compared to intra-myocardial injection of normoglycemic cells, chronic hyperglycemia attenuated cell-mediated improvements in myocardial function and reduced the ability of transplanted cells to promote new blood vessel and cardiomyocyte growth. In contrast, Glo1 overexpression decreased oxidative damage while restoring both cell culture yields and EDC-mediated repair of ischemic myocardium. The latter was associated with enhanced production of pro-healing extracellular vesicles by Glo1 cells without altering the pro-healing microRNA cargo within. <b>Conclusions:</b>
 Chronic hyperglycemia decreases the regenerative performance of EDCs. Overexpression of Glo1 reduces dicarbonyl stress and prevents chronic hyperglycemia-induced dysfunction by rejuvenating the production of pro-healing extracellular vesicles.</AbstractText>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Villanueva</LastName>
<ForeName>Melanie</ForeName>
<Initials>M</Initials>
<AffiliationInfo><Affiliation>University of Ottawa Heart Institute, Division of Cardiology, Department of Medicine, University of Ottawa, Ottawa, Canada K1Y4W7.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Michie</LastName>
<ForeName>Connor</ForeName>
<Initials>C</Initials>
<AffiliationInfo><Affiliation>University of Ottawa Heart Institute, Division of Cardiology, Department of Medicine, University of Ottawa, Ottawa, Canada K1Y4W7.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Parent</LastName>
<ForeName>Sandrine</ForeName>
<Initials>S</Initials>
<AffiliationInfo><Affiliation>University of Ottawa Heart Institute, Division of Cardiology, Department of Medicine, University of Ottawa, Ottawa, Canada K1Y4W7.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Kanaan</LastName>
<ForeName>Georges N</ForeName>
<Initials>GN</Initials>
<AffiliationInfo><Affiliation>Department of Biochemistry, Microbiology and Immunology, Faculty of Medicine, University of Ottawa, Ottawa, Canada K1H8M5.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Rafatian</LastName>
<ForeName>Ghazaleh</ForeName>
<Initials>G</Initials>
<AffiliationInfo><Affiliation>University of Ottawa Heart Institute, Division of Cardiology, Department of Medicine, University of Ottawa, Ottawa, Canada K1Y4W7.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Kanda</LastName>
<ForeName>Pushpinder</ForeName>
<Initials>P</Initials>
<AffiliationInfo><Affiliation>University of Ottawa Heart Institute, Division of Cardiology, Department of Medicine, University of Ottawa, Ottawa, Canada K1Y4W7.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Ye</LastName>
<ForeName>Bin</ForeName>
<Initials>B</Initials>
<AffiliationInfo><Affiliation>University of Ottawa Heart Institute, Division of Cardiology, Department of Medicine, University of Ottawa, Ottawa, Canada K1Y4W7.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Liang</LastName>
<ForeName>Wenbin</ForeName>
<Initials>W</Initials>
<AffiliationInfo><Affiliation>University of Ottawa Heart Institute, Division of Cardiology, Department of Medicine, University of Ottawa, Ottawa, Canada K1Y4W7.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Department of Cellular and Molecular Medicine, Faculty of Medicine, University of Ottawa, Ottawa, Canada K1H8M5.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Harper</LastName>
<ForeName>Mary-Ellen</ForeName>
<Initials>ME</Initials>
<AffiliationInfo><Affiliation>Department of Biochemistry, Microbiology and Immunology, Faculty of Medicine, University of Ottawa, Ottawa, Canada K1H8M5.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Davis</LastName>
<ForeName>Darryl R</ForeName>
<Initials>DR</Initials>
<AffiliationInfo><Affiliation>University of Ottawa Heart Institute, Division of Cardiology, Department of Medicine, University of Ottawa, Ottawa, Canada K1Y4W7.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Department of Cellular and Molecular Medicine, Faculty of Medicine, University of Ottawa, Ottawa, Canada K1H8M5.</Affiliation>
</AffiliationInfo>
</Author>
</AuthorList>
<Language>eng</Language>
<GrantList CompleteYN="Y"><Grant><GrantID>FDN143278</GrantID>
<Agency>CIHR</Agency>
<Country>Canada</Country>
</Grant>
<Grant><GrantID>MC2-121291</GrantID>
<Agency>CIHR</Agency>
<Country>Canada</Country>
</Grant>
</GrantList>
<PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType>
<PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType>
</PublicationTypeList>
<ArticleDate DateType="Electronic"><Year>2019</Year>
<Month>08</Month>
<Day>09</Day>
</ArticleDate>
</Article>
<MedlineJournalInfo><Country>Australia</Country>
<MedlineTA>Theranostics</MedlineTA>
<NlmUniqueID>101552395</NlmUniqueID>
<ISSNLinking>1838-7640</ISSNLinking>
</MedlineJournalInfo>
<ChemicalList><Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D000975">Antioxidants</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D017382">Reactive Oxygen Species</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 4.4.1.5</RegistryNumber>
<NameOfSubstance UI="C000597196">GLO1 protein, human</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 4.4.1.5</RegistryNumber>
<NameOfSubstance UI="D007791">Lactoylglutathione Lyase</NameOfSubstance>
</Chemical>
</ChemicalList>
<CitationSubset>IM</CitationSubset>
<MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000975" MajorTopicYN="N">Antioxidants</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D064987" MajorTopicYN="N">Cell- and Tissue-Based Therapy</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D002908" MajorTopicYN="N">Chronic Disease</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D048909" MajorTopicYN="Y">Diabetes Complications</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000067128" MajorTopicYN="N">Extracellular Vesicles</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D006333" MajorTopicYN="N">Heart Failure</DescriptorName>
<QualifierName UI="Q000201" MajorTopicYN="Y">enzymology</QualifierName>
<QualifierName UI="Q000517" MajorTopicYN="N">prevention & control</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D006943" MajorTopicYN="N">Hyperglycemia</DescriptorName>
<QualifierName UI="Q000150" MajorTopicYN="Y">complications</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D007791" MajorTopicYN="N">Lactoylglutathione Lyase</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008810" MajorTopicYN="N">Mice, Inbred C57BL</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008822" MajorTopicYN="N">Mice, Transgenic</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D009203" MajorTopicYN="N">Myocardial Infarction</DescriptorName>
<QualifierName UI="Q000201" MajorTopicYN="Y">enzymology</QualifierName>
<QualifierName UI="Q000209" MajorTopicYN="N">etiology</QualifierName>
<QualifierName UI="Q000517" MajorTopicYN="N">prevention & control</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D018384" MajorTopicYN="N">Oxidative Stress</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D017382" MajorTopicYN="N">Reactive Oxygen Species</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
</MeshHeadingList>
<KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="Y">cardiac stem cells</Keyword>
<Keyword MajorTopicYN="Y">diabetes</Keyword>
<Keyword MajorTopicYN="Y">extracellular vesicles</Keyword>
<Keyword MajorTopicYN="Y">heart failure</Keyword>
<Keyword MajorTopicYN="Y">hyperglycemia</Keyword>
<Keyword MajorTopicYN="Y">myocardial infarction</Keyword>
<Keyword MajorTopicYN="Y">oxidative stress</Keyword>
<Keyword MajorTopicYN="Y">reactive dicarbonyls</Keyword>
</KeywordList>
<CoiStatement>Competing Interests: The authors have declared that no competing interest exists.</CoiStatement>
</MedlineCitation>
<PubmedData><History><PubMedPubDate PubStatus="received"><Year>2019</Year>
<Month>05</Month>
<Day>13</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="accepted"><Year>2019</Year>
<Month>07</Month>
<Day>06</Day>
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<Day>20</Day>
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<affiliations><list><country><li>Canada</li>
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<name sortKey="Davis, Darryl R" sort="Davis, Darryl R" uniqKey="Davis D" first="Darryl R" last="Davis">Darryl R. Davis</name>
<name sortKey="Harper, Mary Ellen" sort="Harper, Mary Ellen" uniqKey="Harper M" first="Mary-Ellen" last="Harper">Mary-Ellen Harper</name>
<name sortKey="Kanaan, Georges N" sort="Kanaan, Georges N" uniqKey="Kanaan G" first="Georges N" last="Kanaan">Georges N. Kanaan</name>
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<name sortKey="Liang, Wenbin" sort="Liang, Wenbin" uniqKey="Liang W" first="Wenbin" last="Liang">Wenbin Liang</name>
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Glyoxalase 1 Prevents Chronic Hyperglycemia Induced Heart-Explant Derived Cell Dysfunction.

Glyoxalase 1 Prevents Chronic Hyperglycemia Induced Heart-Explant Derived Cell Dysfunction.

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