Evidence map›Paper›PMID 30769031›Full record

ArticleReproductive toxicology (Elmsford, N.Y.)2019

Trehalose restores functional autophagy suppressed by high glucose.

Cheng Xu, Xi Chen, Wei-Bin Sheng, Peixin Yang

RetractedOpen access · greenAbstract readRetracted Publication
In one paragraph

Article in Reproductive toxicology (Elmsford, N.Y.), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.6field-weighted citation impact, top 11% 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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

15 citing papers in PubMed, 37 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Understanding the role of trehalose in interactions betweenFrontiers in cellular and infection microbiology · 2025
    Review
  5. Review
  6. Article
  7. Review
  8. Trehalose Treatment in Zebrafish Model of Lafora Disease.International journal of molecular sciences · 2022
    Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Using trehalose to prevent and treat metabolic function: effectiveness and mechanisms.Current opinion in clinical nutrition and metabolic care · 2019
    Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Cheng XuDepartment of Obstetrics, Gynecology & Reproductive Sciences, Baltimore, MD, USA.
Xi ChenDepartment of Obstetrics, Gynecology & Reproductive Sciences, Baltimore, MD, USA.
Wei-Bin ShengDepartment of Obstetrics, Gynecology & Reproductive Sciences, Baltimore, MD, USA.
Peixin YangDepartment of Obstetrics, Gynecology & Reproductive Sciences, Baltimore, MD, USA; Department of Biochemistry & Molecular Biology, University of Maryland School of Medicine, Baltimore, Maryland, USA. Electronic address: pyang@fpi.umaryland.edu.
University of Maryland, Baltimore · US

Funding

Apoptotic Mechanism of Maternal Diabetes-Induced Neural Tube DefectsR01DK083243 · NIDDK · UNIVERSITY OF MARYLAND BALTIMORE · PI YANG, PEIXIN · 2010 to 2019
$3.1M
Molecular Signalling Pathways and Cellular Stress in Diabetic EmbryopathyR01HD100195 · NICHD · UNIVERSITY OF MARYLAND BALTIMORE · PI REECE, E. ALBERT, YANG, PEIXIN · 2019 to 2023
$2.5M
MicroRNA-Suppressed Mitochondrial Fusion in Mediating the Teratogenicity of Maternal Diabetes Leading to Heart DefectsR01HL134368 · NHLBI · UNIVERSITY OF MARYLAND BALTIMORE · PI WANG, JIAN-YING, YANG, PEIXIN · 2017 to 2020
$2.4M
Maternal Diabetes-Suppressed Vascular Signaling Induces Vasculopathy and Neural Tube DefectsR01HL131737 · NHLBI · UNIVERSITY OF MARYLAND BALTIMORE · PI YANG, PEIXIN · 2016 to 2019
$2.1M
Molecular Signalling Pathways and Cellular Stress in Diabetic EmbryopathyR01DK103024 · NIDDK · UNIVERSITY OF MARYLAND BALTIMORE · PI REECE, E. ALBERT, YANG, PEIXIN · 2014 to 2017
$1.7M
Autophagy and its Regulation in Diabetic EmbryopathyR01DK101972 · NIDDK · UNIVERSITY OF MARYLAND BALTIMORE · PI YANG, PEIXIN · 2014 to 2017
$1.6M
NHLBI NIH HHS R01 HL131737NHLBI NIH HHS R01 HL134368NICHD NIH HHS R01 HD100195NIDDK NIH HHS R01 DK083243NIDDK NIH HHS R01 DK101972NIDDK NIH HHS R01 DK103024
6 · The paper itself

Abstract

Autophagy is required for neurulation, and autophagy activators with minimal toxicity, such as the natural compound trehalose, a nonreducing disaccharide, possess high therapeutic value. To determine whether trehalose directly induces autophagy, FITC-labeled trehalose was used for tracing its presence in autophagosome complexes. Trehalose was as potent as rapamycin and starvation in inducing de novo autophagosome formation and increasing autophagosome flux in GFP-LC3 reporter cells and C17.2 neural stem cells. Trehalose effectively reversed high glucose-suppressed autophagy and reduced p62 protein expression. Trehalose abolished the disruption of autophagosome complexes under high glucose conditions in vitro and maternal diabetes in vivo. Autophagosomes induced by trehalose were functionally active, forming mitophagy and reticulophagy in removing damaged cellular organelles in neuroepithelial cells exposed to maternal diabetes. Thus, trehalose directly participated in functional autophagosome generation by incorporating itself into autophagosomes. These findings provide the mechanistic basis for the use of trehalose in preventing disruptive autophagy-associated pathogenesis.

Indexed as

AnimalsAutophagosomesAutophagyCell LineGlucoseHumansHyperglycemiaMiceNeural Stem CellsTrehaloseGlucoseTrehaloseAutophagosomeAutophagyHigh glucoseMaternal p62diabetesNeural tube defectsTrehalose

Identifiers

PMID30769031
PMCPMC7271258
OpenAlexW2912236790

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.