Evidence map›Paper›PMID 28240313›Full record

ArticleScientific reports2017

Enhancing lysosomal biogenesis and autophagic flux by activating the transcription factor EB protects against cadmium-induced neurotoxicity.

Huifeng Pi, Min Li, Li Tian, Zhiqi Yang, Zhengping Yu, Zhou Zhou

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
5.7field-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

41 citing papers in PubMed, 79 citations in OpenAlex.

  1. Article
  2. Chronic exposure to low levels of glyphosate and metals induces kidney dysfunction.Toxicological sciences : an official journal of the Society of Toxicology · 2026
    Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Cadmium toxicity and autophagy: a review.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2024
    Review
  10. Article
  11. Article
  12. Article
  13. Caveolae with serotonin and NMDA receptors as promising targets for the treatment of Alzheimer's disease.International journal of physiology, pathophysiology and pharmacology · 2024
    Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Lysosomal CaNature communications · 2022
    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

6 authors at 2 institutions in 1 country.

Huifeng PiDepartment of Occupational Health, Third Military Medical University, Chongqing 400038, People's Republic of China.
Min LiDepartment of Occupational Health, Third Military Medical University, Chongqing 400038, People's Republic of China.
Li TianDepartment of Occupational Health, Third Military Medical University, Chongqing 400038, People's Republic of China.
Zhiqi YangBrain Research Center, Third Military Medical University, Chongqing 400038, People's Republic of China.
Zhengping YuDepartment of Occupational Health, Third Military Medical University, Chongqing 400038, People's Republic of China.
Zhou ZhouDepartment of Occupational Health, Third Military Medical University, Chongqing 400038, People's Republic of China.
Army Medical University · CNGuangxi University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cadmium (Cd), a highly ubiquitous heavy metal, is a well-known inducer of neurotoxicity. However, the mechanism underlying cadmium-induced neurotoxicity remains unclear. In this study, we found that Cd inhibits autophagosome-lysosome fusion and impairs lysosomal function by reducing the levels of lysosomal-associated membrane proteins, inhibiting lysosomal proteolysis and altering lysosomal pH, contributing to defects in autophagic clearance and subsequently leading to nerve cell death. In addition, Cd decreases transcription factor EB (TFEB) expression at both the mRNA and protein levels. Furthermore, Cd induces the nuclear translocation of TFEB and TFEB target-gene expression, associated with compromised lysosomal function or a compensatory effect after the impairment of the autophagic flux. Notably, restoration of the levels of lysosomal-associated membrane protein, lysosomal proteolysis, lysosomal pH and autophagic flux through Tfeb overexpression protects against Cd-induced neurotoxicity, and this protective effect is incompletely dependent on TFEB nuclear translocation. Moreover, gene transfer of the master autophagy regulator TFEB results in the clearance of toxic proteins and the correction of Cd-induced neurotoxicity in vivo. Our study is the first to demonstrate that Cd disrupts lysosomal function and autophagic flux and manipulation of TFEB signalling may be a therapeutic approach for antagonizing Cd-induced neurotoxicity.

Indexed as

AnimalsAutophagyBasic Helix-Loop-Helix Leucine Zipper Transcription FactorsCadmiumCathepsin DCell Line, TumorCell NucleusGene Expression RegulationHydrogen-Ion ConcentrationLysosomal-Associated Membrane Protein 1Lysosomal Membrane ProteinsLysosomesMaleMiceMice, Inbred C57BLMicrotubule-Associated ProteinsBasic Helix-Loop-Helix Leucine Zipper Transcription FactorsCadmiumCathepsin DCtsd protein, mouseLamp1 protein, mouseLysosomal-Associated Membrane Protein 1Lysosomal Membrane ProteinsMap1lc3b protein, mouseMicrotubule-Associated ProteinsTcfeb protein, mouse

Identifiers

PMID28240313
PMCPMC5327481
OpenAlexW2594182787

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.