Evidence map›Paper›PMID 32785678›Full record

ArticleInvestigative ophthalmology & visual science2020

Trehalose Induces Autophagy Against Inflammation by Activating TFEB Signaling Pathway in Human Corneal Epithelial Cells Exposed to Hyperosmotic Stress.

Zhao Liu, Ding Chen, Xin Chen, Fang Bian, Wenjuan Qin, Ning Gao, Yangyan Xiao, Jinmiao Li, Stephen C Pflugfelder, De-Quan Li

Open access · goldAbstract read
In one paragraph

Article in Investigative ophthalmology & visual science, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed, 1 pooled it
6.1field-weighted citation impact, top 3% 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

39 citing papers in PubMed, 1 synthesis or guideline pooled it, 54 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Review
  5. Review
  6. Article
  7. Autophagy in ocular diseases: from mechanisms to therapeutic potential.Frontiers in cell and developmental biology · 2026
    Review
  8. Article
  9. Article
  10. Hydroxypropyl-Methylcellulose and GlicoProOphthalmology and therapy · 2025
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Biological Properties ofAntioxidants (Basel, Switzerland) · 2024
    Article
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors at 3 institutions in 2 countries.

Zhao LiuOcular Surface Center, Cullen Eye Institute, Department of Ophthalmology, Baylor College of Medicine, Houston, Texas, United States.
Ding ChenOcular Surface Center, Cullen Eye Institute, Department of Ophthalmology, Baylor College of Medicine, Houston, Texas, United States.
Xin ChenOcular Surface Center, Cullen Eye Institute, Department of Ophthalmology, Baylor College of Medicine, Houston, Texas, United States.
Fang BianOcular Surface Center, Cullen Eye Institute, Department of Ophthalmology, Baylor College of Medicine, Houston, Texas, United States.
Wenjuan QinOcular Surface Center, Cullen Eye Institute, Department of Ophthalmology, Baylor College of Medicine, Houston, Texas, United States.
Ning GaoOcular Surface Center, Cullen Eye Institute, Department of Ophthalmology, Baylor College of Medicine, Houston, Texas, United States.
Yangyan XiaoOcular Surface Center, Cullen Eye Institute, Department of Ophthalmology, Baylor College of Medicine, Houston, Texas, United States.
Jinmiao LiOcular Surface Center, Cullen Eye Institute, Department of Ophthalmology, Baylor College of Medicine, Houston, Texas, United States.
Stephen C PflugfelderOcular Surface Center, Cullen Eye Institute, Department of Ophthalmology, Baylor College of Medicine, Houston, Texas, United States.
De-Quan LiOcular Surface Center, Cullen Eye Institute, Department of Ophthalmology, Baylor College of Medicine, Houston, Texas, United States.
Ocular Surface Center · USBaylor College of Medicine · USWenzhou Medical University · CN

Funding

VISION RESEARCH CENTERP30EY002520 · NEI · BAYLOR COLLEGE OF MEDICINE · PI Samuel M Wu · 1985 to 2026
$14.8M
PATHOGENESIS OF CONJUNCTIVAL SQUAMOUS METAPLASIAR01EY011915 · NEI · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI PFLUGFELDER, STEPHEN C · 1997 to 2023
$8.0M
TLR4-DEPENDENT INNATE IMMUNITY IN POLLEN-TRIGGERED OCULAR ALLERGIC INFLAMMATIONR01EY023598 · NEI · BAYLOR COLLEGE OF MEDICINE · PI LI, DE-QUAN · 2014 to 2018
$2.1M
NEI NIH HHS P30 EY002520NEI NIH HHS R01 EY011915NEI NIH HHS R01 EY023598
6 · The paper itself

Abstract

Purpose: Autophagy plays an important role in balancing the inflammatory response to restore homeostasis. The aim of this study was to explore the mechanism by which trehalose suppresses inflammatory cytokines via autophagy activation in primary human corneal epithelial cells (HCECs) exposed to hyperosmotic stress. Methods: An in vitro dry eye model was used in which HCECs were cultured in hyperosmolar medium with the addition of sodium chloride (NaCl). Trehalose was applied in different concentrations. The levels of TNF-α, IL-1β, IL-6, and IL-8 were detected using RT-qPCR and ELISA. Cell viability assays, immunofluorescent staining of LC3B, and western blots of Beclin1, Atg5, Atg7, LC3B, and P62 were conducted. The key factors in upstream signaling pathways of autophagy activation were measured: P-Akt, Akt, and transcription factor EB (TFEB). Results: Trehalose reduced the proinflammatory mediators TNF-α, IL-1β, IL-6, and IL-8 in primary HCECs at 450 mOsM. This effect was osmolarity dependent, and a level of 1.0% trehalose showed the most suppression. Trehalose promoted autophagosome formation and autophagic flux, as evidenced by increased production of Beclin1, Atg5, and Atg7, as well as higher LC3B I protein turnover to LC3B II, with decreased protein levels of P62/SQSTM1. The addition of 3-methyladenine blocked autophagy activation and increased the release of proinflammatory cytokines. Trehalose further activated TFEB, with translocation from cytoplasm to the nucleus, but diminished Akt activity. Conclusions: Our findings demonstrate that trehalose, functioning as an autophagy enhancer, suppresses the inflammatory response by promoting autophagic flux via TFEB activation in primary HCECs exposed to hyperosmotic stress, a process that is beneficial to dry eye.

Indexed as

AdolescentAdultAgedAutophagyBasic Helix-Loop-Helix Leucine Zipper Transcription FactorsCells, CulturedDose-Response Relationship, DrugEnzyme-Linked Immunosorbent AssayEpithelium, CornealHumansInflammationInterleukin-1betaInterleukin-6Interleukin-8Middle AgedOsmotic PressureBasic Helix-Loop-Helix Leucine Zipper Transcription FactorsInterleukin-1betaInterleukin-6Interleukin-8TFEB protein, humanTrehaloseTumor Necrosis Factor-alpha

Identifiers

PMID32785678
PMCPMC7441355
OpenAlexW3048882742

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.