Trehalose-Induced Activation of Autophagy Improves Cardiac Remodeling After Myocardial Infarction.
Identifieur interne : 000111 ( PubMed/Corpus ); précédent : 000110; suivant : 000112Trehalose-Induced Activation of Autophagy Improves Cardiac Remodeling After Myocardial Infarction.
Auteurs : Sebastiano Sciarretta ; Derek Yee ; Narayani Nagarajan ; Franca Bianchi ; Toshiro Saito ; Valentina Valenti ; Mingming Tong ; Dominic P. Del Re ; Carmine Vecchione ; Leonardo Schirone ; Maurizio Forte ; Speranza Rubattu ; Akihiro Shirakabe ; V Subbarao Boppana ; Massimo Volpe ; Giacomo Frati ; Peiyong Zhai ; Junichi SadoshimaSource :
- Journal of the American College of Cardiology [ 1558-3597 ] ; 2018.
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 to Exploration step
pubmed:29724354Le document en format XML
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<author><name sortKey="Frati, Giacomo" sort="Frati, Giacomo" uniqKey="Frati G" first="Giacomo" last="Frati">Giacomo Frati</name>
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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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<author><name sortKey="Nagarajan, Narayani" sort="Nagarajan, Narayani" uniqKey="Nagarajan N" first="Narayani" last="Nagarajan">Narayani Nagarajan</name>
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<author><name sortKey="Bianchi, Franca" sort="Bianchi, Franca" uniqKey="Bianchi F" first="Franca" last="Bianchi">Franca Bianchi</name>
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<author><name sortKey="Saito, Toshiro" sort="Saito, Toshiro" uniqKey="Saito T" first="Toshiro" last="Saito">Toshiro Saito</name>
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<author><name sortKey="Valenti, Valentina" sort="Valenti, Valentina" uniqKey="Valenti V" first="Valentina" last="Valenti">Valentina Valenti</name>
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<author><name sortKey="Tong, Mingming" sort="Tong, Mingming" uniqKey="Tong M" first="Mingming" last="Tong">Mingming Tong</name>
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<author><name sortKey="Del Re, Dominic P" sort="Del Re, Dominic P" uniqKey="Del Re D" first="Dominic P" last="Del Re">Dominic P. Del Re</name>
<affiliation><nlm:affiliation>Department of Cell Biology and Molecular Medicine, Rutgers New Jersey Medical School, Newark, New Jersey.</nlm:affiliation>
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<author><name sortKey="Vecchione, Carmine" sort="Vecchione, Carmine" uniqKey="Vecchione C" first="Carmine" last="Vecchione">Carmine Vecchione</name>
<affiliation><nlm:affiliation>Department of AngioCardioNeurology, IRCCS Neuromed, Pozzilli, Italy; University of Salerno, Medicine and Surgery, Baronissi, Italy.</nlm:affiliation>
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<author><name sortKey="Schirone, Leonardo" sort="Schirone, Leonardo" uniqKey="Schirone L" first="Leonardo" last="Schirone">Leonardo Schirone</name>
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<author><name sortKey="Forte, Maurizio" sort="Forte, Maurizio" uniqKey="Forte M" first="Maurizio" last="Forte">Maurizio Forte</name>
<affiliation><nlm:affiliation>Department of AngioCardioNeurology, IRCCS Neuromed, Pozzilli, Italy.</nlm:affiliation>
</affiliation>
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<author><name sortKey="Rubattu, Speranza" sort="Rubattu, Speranza" uniqKey="Rubattu S" first="Speranza" last="Rubattu">Speranza Rubattu</name>
<affiliation><nlm:affiliation>Department of AngioCardioNeurology, IRCCS Neuromed, Pozzilli, Italy; Department of Clinical and Molecular Medicine, Sapienza University of Rome, Rome, Italy.</nlm:affiliation>
</affiliation>
</author>
<author><name sortKey="Shirakabe, Akihiro" sort="Shirakabe, Akihiro" uniqKey="Shirakabe A" first="Akihiro" last="Shirakabe">Akihiro Shirakabe</name>
<affiliation><nlm:affiliation>Department of Cell Biology and Molecular Medicine, Rutgers New Jersey Medical School, Newark, New Jersey.</nlm:affiliation>
</affiliation>
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<author><name sortKey="Boppana, V Subbarao" sort="Boppana, V Subbarao" uniqKey="Boppana V" first="V Subbarao" last="Boppana">V Subbarao Boppana</name>
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<author><name sortKey="Volpe, Massimo" sort="Volpe, Massimo" uniqKey="Volpe M" first="Massimo" last="Volpe">Massimo Volpe</name>
<affiliation><nlm:affiliation>Department of AngioCardioNeurology, IRCCS Neuromed, Pozzilli, Italy; Department of Clinical and Molecular Medicine, Sapienza University of Rome, Rome, Italy.</nlm:affiliation>
</affiliation>
</author>
<author><name sortKey="Frati, Giacomo" sort="Frati, Giacomo" uniqKey="Frati G" first="Giacomo" last="Frati">Giacomo Frati</name>
<affiliation><nlm:affiliation>Department of Medico-Surgical Sciences and Biotechnologies, Sapienza University of Rome, Latina, Italy; Department of AngioCardioNeurology, IRCCS Neuromed, Pozzilli, Italy.</nlm:affiliation>
</affiliation>
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<author><name sortKey="Zhai, Peiyong" sort="Zhai, Peiyong" uniqKey="Zhai P" first="Peiyong" last="Zhai">Peiyong Zhai</name>
<affiliation><nlm:affiliation>Department of Cell Biology and Molecular Medicine, Rutgers New Jersey Medical School, Newark, New Jersey.</nlm:affiliation>
</affiliation>
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<author><name sortKey="Sadoshima, Junichi" sort="Sadoshima, Junichi" uniqKey="Sadoshima J" first="Junichi" last="Sadoshima">Junichi Sadoshima</name>
<affiliation><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>
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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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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term>
<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="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Basic Helix-Loop-Helix Leucine Zipper Transcription Factors</term>
</keywords>
<keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Autophagy</term>
<term>Heart</term>
<term>Ventricular Remodeling</term>
</keywords>
<keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Myocardial Infarction</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Trehalose</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Animals</term>
<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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<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>
</TEI>
<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>
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