ChloroquineV1, Ncbi, Merge, bibRecord, 000442

Trehalose-Induced Activation of Autophagy Improves Cardiac Remodeling After Myocardial Infarction.

Identifieur interne : 000442 ( Ncbi/Merge ); précédent : 000441; suivant : 000443

Trehalose-Induced Activation of Autophagy Improves Cardiac Remodeling After Myocardial Infarction.

Auteurs : Sebastiano Sciarretta [Italie] ; Derek Yee [États-Unis] ; Narayani Nagarajan [États-Unis] ; Franca Bianchi [Italie] ; Toshiro Saito [États-Unis] ; Valentina Valenti [Italie] ; Mingming Tong [États-Unis] ; Dominic P. Del Re [États-Unis] ; Carmine Vecchione [Italie] ; Leonardo Schirone [Italie] ; Maurizio Forte [Italie] ; Speranza Rubattu [Italie] ; Akihiro Shirakabe [États-Unis] ; V Subbarao Boppana [États-Unis] ; Massimo Volpe [Italie] ; Giacomo Frati [Italie] ; Peiyong Zhai [États-Unis] ; Junichi Sadoshima [États-Unis]

Source :

Journal of the American College of Cardiology [ 1558-3597 ] ; 2018.

RBID : pubmed:29724354

Descripteurs français

KwdFr :
- Animaux, Animaux nouveau-nés, Autophagie (), Cellules cultivées, Coeur (), Facteurs de transcription à motifs basiques hélice-boucle-hélice et à glissière à leucines (métabolisme), Infarctus du myocarde (traitement médicamenteux), Modèles animaux de maladie humaine, Rats, Remodelage ventriculaire (), Souris transgéniques, Tréhalose (usage thérapeutique), Évaluation préclinique de médicament.
MESH :
- métabolisme : Facteurs de transcription à motifs basiques hélice-boucle-hélice et à glissière à leucines.
- traitement médicamenteux : Infarctus du myocarde.
- usage thérapeutique : Tréhalose.
- Animaux, Animaux nouveau-nés, Autophagie, Cellules cultivées, Coeur, Modèles animaux de maladie humaine, Rats, Remodelage ventriculaire, Souris transgéniques, Évaluation préclinique de médicament.

English descriptors

KwdEn :
- Animals, Animals, Newborn, Autophagy (drug effects), Basic Helix-Loop-Helix Leucine Zipper Transcription Factors (metabolism), Cells, Cultured, Disease Models, Animal, Drug Evaluation, Preclinical, Heart (drug effects), Mice, Transgenic, Myocardial Infarction (drug therapy), Rats, Trehalose (therapeutic use), Ventricular Remodeling (drug effects).
MESH :
- chemical , metabolism : Basic Helix-Loop-Helix Leucine Zipper Transcription Factors.
- drug effects : Autophagy, Heart, Ventricular Remodeling.
- drug therapy : Myocardial Infarction.
- chemical , therapeutic use : Trehalose.
- Animals, Animals, Newborn, Cells, Cultured, Disease Models, Animal, Drug Evaluation, Preclinical, Mice, Transgenic, Rats.

Abstract

Trehalose (TRE) is a natural, nonreducing disaccharide synthesized by lower organisms. TRE exhibits an extraordinary ability to protect cells against different kinds of stresses through activation of autophagy. However, the effect of TRE on the heart during stress has never been tested.

DOI: 10.1016/j.jacc.2018.02.066
PubMed: 29724354

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

to stream PubMed, to step Corpus: 000111
to stream PubMed, to step Curation: 000111
to stream PubMed, to step Checkpoint: 000082

Links to Exploration step

pubmed:29724354

Le document en format XML

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<sourceDesc><biblStruct><analytic><title xml:lang="en">Trehalose-Induced Activation of Autophagy Improves Cardiac Remodeling After Myocardial Infarction.</title>
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<country xml:lang="fr">Italie</country>
<wicri:regionArea>Department of AngioCardioNeurology, IRCCS Neuromed, Pozzilli, Italy; Department of Clinical and Molecular Medicine, Sapienza University of Rome, Rome</wicri:regionArea>
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<country xml:lang="fr">États-Unis</country>
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<country xml:lang="fr">Italie</country>
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<country xml:lang="fr">Italie</country>
<wicri:regionArea>Department of Medico-Surgical Sciences and Biotechnologies, Sapienza University of Rome, Latina, Italy; Department of AngioCardioNeurology, IRCCS Neuromed, Pozzilli</wicri:regionArea>
<wicri:noRegion>Pozzilli</wicri:noRegion>
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<author><name sortKey="Zhai, Peiyong" sort="Zhai, Peiyong" uniqKey="Zhai P" first="Peiyong" last="Zhai">Peiyong Zhai</name>
<affiliation wicri:level="2"><nlm:affiliation>Department of Cell Biology and Molecular Medicine, Rutgers New Jersey Medical School, Newark, New Jersey.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<placeName><region type="state">New Jersey</region>
</placeName>
<wicri:cityArea>Department of Cell Biology and Molecular Medicine, Rutgers New Jersey Medical School, Newark</wicri:cityArea>
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<author><name sortKey="Sadoshima, Junichi" sort="Sadoshima, Junichi" uniqKey="Sadoshima J" first="Junichi" last="Sadoshima">Junichi Sadoshima</name>
<affiliation wicri:level="2"><nlm:affiliation>Department of Cell Biology and Molecular Medicine, Rutgers New Jersey Medical School, Newark, New Jersey. Electronic address: sadoshju@njms.rutgers.edu.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<placeName><region type="state">New Jersey</region>
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<series><title level="j">Journal of the American College of Cardiology</title>
<idno type="eISSN">1558-3597</idno>
<imprint><date when="2018" type="published">2018</date>
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<term>Animals, Newborn</term>
<term>Autophagy (drug effects)</term>
<term>Basic Helix-Loop-Helix Leucine Zipper Transcription Factors (metabolism)</term>
<term>Cells, Cultured</term>
<term>Disease Models, Animal</term>
<term>Drug Evaluation, Preclinical</term>
<term>Heart (drug effects)</term>
<term>Mice, Transgenic</term>
<term>Myocardial Infarction (drug therapy)</term>
<term>Rats</term>
<term>Trehalose (therapeutic use)</term>
<term>Ventricular Remodeling (drug effects)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term>
<term>Animaux nouveau-nés</term>
<term>Autophagie ()</term>
<term>Cellules cultivées</term>
<term>Coeur ()</term>
<term>Facteurs de transcription à motifs basiques hélice-boucle-hélice et à glissière à leucines (métabolisme)</term>
<term>Infarctus du myocarde (traitement médicamenteux)</term>
<term>Modèles animaux de maladie humaine</term>
<term>Rats</term>
<term>Remodelage ventriculaire ()</term>
<term>Souris transgéniques</term>
<term>Tréhalose (usage thérapeutique)</term>
<term>Évaluation préclinique de médicament</term>
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<term>Heart</term>
<term>Ventricular Remodeling</term>
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<keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Myocardial Infarction</term>
</keywords>
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<term>Animals, Newborn</term>
<term>Cells, Cultured</term>
<term>Disease Models, Animal</term>
<term>Drug Evaluation, Preclinical</term>
<term>Mice, Transgenic</term>
<term>Rats</term>
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<term>Animaux nouveau-nés</term>
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<term>Modèles animaux de maladie humaine</term>
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<front><div type="abstract" xml:lang="en">Trehalose (TRE) is a natural, nonreducing disaccharide synthesized by lower organisms. TRE exhibits an extraordinary ability to protect cells against different kinds of stresses through activation of autophagy. However, the effect of TRE on the heart during stress has never been tested.</div>
</front>
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<pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">29724354</PMID>
<DateCompleted><Year>2019</Year>
<Month>07</Month>
<Day>29</Day>
</DateCompleted>
<DateRevised><Year>2020</Year>
<Month>03</Month>
<Day>06</Day>
</DateRevised>
<Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1558-3597</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>71</Volume>
<Issue>18</Issue>
<PubDate><Year>2018</Year>
<Month>05</Month>
<Day>08</Day>
</PubDate>
</JournalIssue>
<Title>Journal of the American College of Cardiology</Title>
<ISOAbbreviation>J. Am. Coll. Cardiol.</ISOAbbreviation>
</Journal>
<ArticleTitle>Trehalose-Induced Activation of Autophagy Improves Cardiac Remodeling After Myocardial Infarction.</ArticleTitle>
<Pagination><MedlinePgn>1999-2010</MedlinePgn>
</Pagination>
<ELocationID EIdType="pii" ValidYN="Y">S0735-1097(18)33611-8</ELocationID>
<ELocationID EIdType="doi" ValidYN="Y">10.1016/j.jacc.2018.02.066</ELocationID>
<Abstract><AbstractText Label="BACKGROUND">Trehalose (TRE) is a natural, nonreducing disaccharide synthesized by lower organisms. TRE exhibits an extraordinary ability to protect cells against different kinds of stresses through activation of autophagy. However, the effect of TRE on the heart during stress has never been tested.</AbstractText>
<AbstractText Label="OBJECTIVES">This study evaluated the effects of TRE administration in a mouse model of chronic ischemic remodeling.</AbstractText>
<AbstractText Label="METHODS">Wild-type (WT) or beclin1+/- mice were subjected to permanent ligation of the left anterior descending artery (LAD) and then treated with either placebo or trehalose (1 mg/g/day intraperitoneally for 48 h, then 2% in the drinking water). After 4 weeks, echocardiographic, hemodynamic, gravimetric, histological, and biochemical analyses were conducted.</AbstractText>
<AbstractText Label="RESULTS">TRE reduced left ventricular (LV) dilation and increased ventricular function in mice with LAD ligation compared with placebo. Sucrose, another nonreducing disaccharide, did not exert protective effects during post-infarction LV remodeling. Trehalose administration to mice overexpressing GFP-tagged LC3 significantly increased the number of GFP-LC3 dots, both in the presence and absence of chloroquine administration. TRE also increased cardiac LC3-II levels after 4 weeks following myocardial infarction (MI), indicating that it induced autophagy in the heart in vivo. To evaluate whether TRE exerted beneficial effects through activation of autophagy, trehalose was administered to beclin 1+/- mice. The improvement of LV function, lung congestion, cardiac remodeling, apoptosis, and fibrosis following TRE treatment observed in WT mice were all significantly blunted in beclin 1+/- mice.</AbstractText>
<AbstractText Label="CONCLUSIONS">TRE reduced MI-induced cardiac remodeling and dysfunction through activation of autophagy.</AbstractText>
<CopyrightInformation>Copyright © 2018 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.</CopyrightInformation>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Sciarretta</LastName>
<ForeName>Sebastiano</ForeName>
<Initials>S</Initials>
<AffiliationInfo><Affiliation>Department of Medico-Surgical Sciences and Biotechnologies, Sapienza University of Rome, Latina, Italy; Department of AngioCardioNeurology, IRCCS Neuromed, Pozzilli, Italy.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Yee</LastName>
<ForeName>Derek</ForeName>
<Initials>D</Initials>
<AffiliationInfo><Affiliation>Department of Cell Biology and Molecular Medicine, Rutgers New Jersey Medical School, Newark, New Jersey.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Nagarajan</LastName>
<ForeName>Narayani</ForeName>
<Initials>N</Initials>
<AffiliationInfo><Affiliation>Department of Cell Biology and Molecular Medicine, Rutgers New Jersey Medical School, Newark, New Jersey.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Bianchi</LastName>
<ForeName>Franca</ForeName>
<Initials>F</Initials>
<AffiliationInfo><Affiliation>Department of AngioCardioNeurology, IRCCS Neuromed, Pozzilli, Italy.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Saito</LastName>
<ForeName>Toshiro</ForeName>
<Initials>T</Initials>
<AffiliationInfo><Affiliation>Department of Cell Biology and Molecular Medicine, Rutgers New Jersey Medical School, Newark, New Jersey.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Valenti</LastName>
<ForeName>Valentina</ForeName>
<Initials>V</Initials>
<AffiliationInfo><Affiliation>Department of Imaging, Bambino Gesù Children Hospital, IRCCS, Rome, Italy.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Tong</LastName>
<ForeName>Mingming</ForeName>
<Initials>M</Initials>
<AffiliationInfo><Affiliation>Department of Cell Biology and Molecular Medicine, Rutgers New Jersey Medical School, Newark, New Jersey.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Del Re</LastName>
<ForeName>Dominic P</ForeName>
<Initials>DP</Initials>
<AffiliationInfo><Affiliation>Department of Cell Biology and Molecular Medicine, Rutgers New Jersey Medical School, Newark, New Jersey.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Vecchione</LastName>
<ForeName>Carmine</ForeName>
<Initials>C</Initials>
<AffiliationInfo><Affiliation>Department of AngioCardioNeurology, IRCCS Neuromed, Pozzilli, Italy; University of Salerno, Medicine and Surgery, Baronissi, Italy.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Schirone</LastName>
<ForeName>Leonardo</ForeName>
<Initials>L</Initials>
<AffiliationInfo><Affiliation>Department of Medico-Surgical Sciences and Biotechnologies, Sapienza University of Rome, Latina, Italy.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Forte</LastName>
<ForeName>Maurizio</ForeName>
<Initials>M</Initials>
<AffiliationInfo><Affiliation>Department of AngioCardioNeurology, IRCCS Neuromed, Pozzilli, Italy.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Rubattu</LastName>
<ForeName>Speranza</ForeName>
<Initials>S</Initials>
<AffiliationInfo><Affiliation>Department of AngioCardioNeurology, IRCCS Neuromed, Pozzilli, Italy; Department of Clinical and Molecular Medicine, Sapienza University of Rome, Rome, Italy.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Shirakabe</LastName>
<ForeName>Akihiro</ForeName>
<Initials>A</Initials>
<AffiliationInfo><Affiliation>Department of Cell Biology and Molecular Medicine, Rutgers New Jersey Medical School, Newark, New Jersey.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Boppana</LastName>
<ForeName>V Subbarao</ForeName>
<Initials>VS</Initials>
<AffiliationInfo><Affiliation>Department of Cell Biology and Molecular Medicine, Rutgers New Jersey Medical School, Newark, New Jersey.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Volpe</LastName>
<ForeName>Massimo</ForeName>
<Initials>M</Initials>
<AffiliationInfo><Affiliation>Department of AngioCardioNeurology, IRCCS Neuromed, Pozzilli, Italy; Department of Clinical and Molecular Medicine, Sapienza University of Rome, Rome, Italy.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Frati</LastName>
<ForeName>Giacomo</ForeName>
<Initials>G</Initials>
<AffiliationInfo><Affiliation>Department of Medico-Surgical Sciences and Biotechnologies, Sapienza University of Rome, Latina, Italy; Department of AngioCardioNeurology, IRCCS Neuromed, Pozzilli, Italy.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Zhai</LastName>
<ForeName>Peiyong</ForeName>
<Initials>P</Initials>
<AffiliationInfo><Affiliation>Department of Cell Biology and Molecular Medicine, Rutgers New Jersey Medical School, Newark, New Jersey.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Sadoshima</LastName>
<ForeName>Junichi</ForeName>
<Initials>J</Initials>
<AffiliationInfo><Affiliation>Department of Cell Biology and Molecular Medicine, Rutgers New Jersey Medical School, Newark, New Jersey. Electronic address: sadoshju@njms.rutgers.edu.</Affiliation>
</AffiliationInfo>
</Author>
</AuthorList>
<Language>eng</Language>
<GrantList CompleteYN="Y"><Grant><GrantID>R01 HL102738</GrantID>
<Acronym>HL</Acronym>
<Agency>NHLBI NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>R01 HL091469</GrantID>
<Acronym>HL</Acronym>
<Agency>NHLBI NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>R01 HL138720</GrantID>
<Acronym>HL</Acronym>
<Agency>NHLBI NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>R01 HL067724</GrantID>
<Acronym>HL</Acronym>
<Agency>NHLBI NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>R01 HL127339</GrantID>
<Acronym>HL</Acronym>
<Agency>NHLBI NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>R01 HL112330</GrantID>
<Acronym>HL</Acronym>
<Agency>NHLBI NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>R01 AG023039</GrantID>
<Acronym>AG</Acronym>
<Agency>NIA NIH HHS</Agency>
<Country>United States</Country>
</Grant>
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<PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType>
<PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType>
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<MedlineTA>J Am Coll Cardiol</MedlineTA>
<NlmUniqueID>8301365</NlmUniqueID>
<ISSNLinking>0735-1097</ISSNLinking>
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</MeshHeading>
<MeshHeading><DescriptorName UI="D000831" MajorTopicYN="N">Animals, Newborn</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D001343" MajorTopicYN="N">Autophagy</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName>
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<MeshHeading><DescriptorName UI="D004195" MajorTopicYN="N">Disease Models, Animal</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D004353" MajorTopicYN="N">Drug Evaluation, Preclinical</DescriptorName>
</MeshHeading>
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<QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008822" MajorTopicYN="N">Mice, Transgenic</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D009203" MajorTopicYN="N">Myocardial Infarction</DescriptorName>
<QualifierName UI="Q000188" MajorTopicYN="Y">drug therapy</QualifierName>
</MeshHeading>
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<MeshHeading><DescriptorName UI="D014199" MajorTopicYN="N">Trehalose</DescriptorName>
<QualifierName UI="Q000627" MajorTopicYN="Y">therapeutic use</QualifierName>
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<KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="Y">autophagy</Keyword>
<Keyword MajorTopicYN="Y">cardiac remodeling</Keyword>
<Keyword MajorTopicYN="Y">heart failure</Keyword>
<Keyword MajorTopicYN="Y">trehalose</Keyword>
<Keyword MajorTopicYN="Y">ventricular function</Keyword>
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   |texte=   Trehalose-Induced Activation of Autophagy Improves Cardiac Remodeling After Myocardial Infarction.
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Trehalose-Induced Activation of Autophagy Improves Cardiac Remodeling After Myocardial Infarction.

Trehalose-Induced Activation of Autophagy Improves Cardiac Remodeling After Myocardial Infarction.

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