Evidence map›Paper›PMID 29724354›Full record

ArticleJournal of the American College of Cardiology2018

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

Sebastiano Sciarretta, Derek Yee, Narayani Nagarajan, Franca Bianchi, Toshiro Saito, Valentina Valenti, Mingming Tong, Dominic P Del Re, Carmine Vecchione, Leonardo Schirone and 8 more

Registry-linked trialOpen access · greenAbstract read
In one paragraph

Article in Journal of the American College of Cardiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04061070 (Effects of Trehalose and a Mix of Polyphenols on Endothelial Function, Oxidative Stress, Platelet Function and Autophagy in Vasculopathic Patients), which is not on this map. Cited by 136 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
136citing papers in PubMed, 2 pooled it
27.2field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

NCT04061070 nacompletednot on this mapstarted 2019, after this paper: background citation

Effects of Trehalose and a Mix of Polyphenols on Endothelial Function, Oxidative Stress, Platelet Function and Autophagy in Vasculopathic Patients

TypeinterventionalSponsorUniversity of Roma La SapienzaRan2019 to 2021Enrolled80ConditionsOxidative Stress, Cardiovascular DiseasesArmsSupplementation with mix of threalose plus polyphenols, No Supplementation with mix of threalose plus polyphenols
3 · Its place in the literature

Who cites it

136 citing papers in PubMed, 2 syntheses or guidelines pooled it, 245 citations in OpenAlex.

  1. Pooled it
  2. Guidelines for in vivo mouse models of myocardial infarction.American journal of physiology. Heart and circulatory physiology · 2021
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76 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

18 authors at 5 institutions in 2 countries.

Sebastiano SciarrettaDepartment of Medico-Surgical Sciences and Biotechnologies, Sapienza University of Rome, Latina, Italy; Department of AngioCardioNeurology, IRCCS Neuromed, Pozzilli, Italy.
Derek YeeDepartment of Cell Biology and Molecular Medicine, Rutgers New Jersey Medical School, Newark, New Jersey.
Narayani NagarajanDepartment of Cell Biology and Molecular Medicine, Rutgers New Jersey Medical School, Newark, New Jersey.
Franca BianchiDepartment of AngioCardioNeurology, IRCCS Neuromed, Pozzilli, Italy.
Toshiro SaitoDepartment of Cell Biology and Molecular Medicine, Rutgers New Jersey Medical School, Newark, New Jersey.
Valentina ValentiDepartment of Imaging, Bambino Gesù Children Hospital, IRCCS, Rome, Italy.
Mingming TongDepartment of Cell Biology and Molecular Medicine, Rutgers New Jersey Medical School, Newark, New Jersey.
Dominic P Del ReDepartment of Cell Biology and Molecular Medicine, Rutgers New Jersey Medical School, Newark, New Jersey.
Carmine VecchioneDepartment of AngioCardioNeurology, IRCCS Neuromed, Pozzilli, Italy; University of Salerno, Medicine and Surgery, Baronissi, Italy.
Leonardo SchironeDepartment of Medico-Surgical Sciences and Biotechnologies, Sapienza University of Rome, Latina, Italy.
Maurizio ForteDepartment of AngioCardioNeurology, IRCCS Neuromed, Pozzilli, Italy.
Speranza RubattuDepartment of AngioCardioNeurology, IRCCS Neuromed, Pozzilli, Italy; Department of Clinical and Molecular Medicine, Sapienza University of Rome, Rome, Italy.
Akihiro ShirakabeDepartment of Cell Biology and Molecular Medicine, Rutgers New Jersey Medical School, Newark, New Jersey.
V Subbarao BoppanaDepartment of Cell Biology and Molecular Medicine, Rutgers New Jersey Medical School, Newark, New Jersey.
Massimo VolpeDepartment of AngioCardioNeurology, IRCCS Neuromed, Pozzilli, Italy; Department of Clinical and Molecular Medicine, Sapienza University of Rome, Rome, Italy.
Giacomo FratiDepartment of Medico-Surgical Sciences and Biotechnologies, Sapienza University of Rome, Latina, Italy; Department of AngioCardioNeurology, IRCCS Neuromed, Pozzilli, Italy.
Peiyong ZhaiDepartment of Cell Biology and Molecular Medicine, Rutgers New Jersey Medical School, Newark, New Jersey.
Junichi SadoshimaDepartment of Cell Biology and Molecular Medicine, Rutgers New Jersey Medical School, Newark, New Jersey. Electronic address: sadoshju@njms.rutgers.edu.
Rutgers, The State University of New Jersey · USIstituto Neurologico Mediterraneo · ITBambino Gesù Children's Hospital · ITSapienza University of Rome · ITUniversity of Salerno · IT

Funding

Cysteine oxidation in the heartR01HL091469 · NHLBI · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI Junichi Sadoshima · 2008 to 2026
$9.4M
The Role of Serine Signaling in Compensatory Cardiac HypertrophyR01HL112330 · NHLBI · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI Junichi Sadoshima · 2012 to 2026
$7.5M
The Role of Thioredoxin in the Aging HeartR01AG023039 · NIA · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI SADOSHIMA, JUNICHI · 2004 to 2018
$5.8M
Regulation of myocardial growth and death by GSK-3R01HL067724 · NHLBI · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI SADOSHIMA, JUNICHI · 2000 to 2018
$5.1M
Removal of damaged mitochondria by alternative autophagyR01HL138720 · NHLBI · RUTGERS BIOMEDICAL AND HEALTH SCIENCES · PI SADOSHIMA, JUNICHI · 2017 to 2024
$4.7M
Regulation of myocardial growth and death by autophagyR01HL102738 · NHLBI · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI SADOSHIMA, JUNICHI · 2010 to 2014
$2.5M
The role of NF2 in myocardial ischemia and reperfusion injuryR01HL127339 · NHLBI · RBHS-NEW JERSEY MEDICAL SCHOOL · PI DEL RE, DOMINIC P · 2015 to 2019
$2.0M
NHLBI NIH HHS R01 HL067724NHLBI NIH HHS R01 HL091469NHLBI NIH HHS R01 HL102738NHLBI NIH HHS R01 HL112330NHLBI NIH HHS R01 HL127339NHLBI NIH HHS R01 HL138720NIA NIH HHS R01 AG023039
6 · The paper itself

Abstract

backgroundTrehalose (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.

objectivesThis study evaluated the effects of TRE administration in a mouse model of chronic ischemic remodeling.

methodsWild-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.

resultsTRE 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.

conclusionsTRE reduced MI-induced cardiac remodeling and dysfunction through activation of autophagy.

Indexed as

AnimalsAnimals, NewbornAutophagyBasic Helix-Loop-Helix Leucine Zipper Transcription FactorsCells, CulturedDisease Models, AnimalDrug Evaluation, PreclinicalHeartMice, TransgenicMyocardial InfarctionRatsTrehaloseVentricular RemodelingBasic Helix-Loop-Helix Leucine Zipper Transcription FactorsTcfeb protein, mouseTFEB protein, ratTrehaloseautophagycardiac remodelingheart failuretrehaloseventricular function

Identifiers

PMID29724354
PMCPMC6347412
OpenAlexW2802954507

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Registered trials

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.