Evidence map›Paper›PMID 17404497›Full record

ArticleAutophagy

The autophagic pathway: a cell survival strategy against the bacterial pore-forming toxin Vibrio cholerae cytolysin.

Héctor A Saka, Maximiliano G Gutiérrez, José L Bocco, María I Colombo

Open access · bronzeAbstract readComment
PubMed Publisher
In one paragraph

Article in Autophagy. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
3.2field-weighted citation impact, top 10% 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

18 citing papers in PubMed, 30 citations in OpenAlex.

  1. Enigmatic roles ofJournal of bacteriology · 2025
    Review
  2. Autophagy in oral cancer: Promises and challenges (Review).International journal of molecular medicine · 2024
    Review
  3. Article
  4. Article
  5. Mechanisms protecting host cells against bacterial pore-forming toxins.Cellular and molecular life sciences : CMLS · 2019
    Review
  6. Review
  7. Article
  8. Article
  9. A Novel Role ofFrontiers in cellular and infection microbiology · 2017
    Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. Autophagy: a primer for the gastroenterologist/hepatologist.Canadian journal of gastroenterology = Journal canadien de gastroenterologie · 2011
    Review
  15. Article
  16. Article
  17. Article
  18. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Héctor A SakaDepartamento de Bioquímica Clínica, Centro de Investigaciones en Bioquímica Clínica e Inmunología (CONICET), Universidad Nacional de Córdoba, Córdoba, Argentina.
Maximiliano G Gutiérrez
José L Bocco
María I Colombo
Universidad Nacional de Córdoba · AR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Vibrio cholerae is the causative agent of cholera in humans. In addition to the criticalvirulence factors cholera toxin and toxin coregulated pilus, V. cholerae secretes V.cholerae cytolysin (VCC), a pore-forming exotoxin able to induce cell lysis and extensivevacuolation. We have shown that this vacuolation is related to the activation of autophagyin response to VCC action. Furthermore, we found that the autophagic pathway wasrequired to protect cells upon VCC intoxication. Based on additional data presented here,we propose a model aimed to explain the mechanism of cell protection. We postulatethat VCC-induced autophagic vacuoles, which display features of multivesicular bodies and enclose the toxin, are implicated in cell defense through VCC degradation involvingfusion with lysosomes.

Indexed as

AnimalsAutophagyCaco-2 CellsCell SurvivalCHO CellsCricetinaeCricetulusHumansLysosomesMembrane GlycoproteinsModels, BiologicalPerforinPore Forming Cytotoxic ProteinsVacuolesVibrio choleraeMembrane GlycoproteinsPerforinPore Forming Cytotoxic Proteins

Identifiers

PMID17404497
OpenAlexW2012865046

What OpenQuestion holds

Textmetadata
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.