Evidence map›Paper›PMID 25114220›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2014

Autophagy protects C. elegans against necrosis during Pseudomonas aeruginosa infection.

Cheng-Gang Zou, Yi-Cheng Ma, Li-Li Dai, Ke-Qin Zhang

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed, 2 pooled it
4.9field-weighted citation impact, top 5% 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

42 citing papers in PubMed, 2 syntheses or guidelines pooled it, 75 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
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  14. Propulsive cell entry diverts pathogens from immune degradation by remodeling the phagocytic synapse.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
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  18. Profile of Prof. Ke-Qin Zhang.Science China. Life sciences · 2023
    Article
  19. Article
  20. The p38 MAPK/PMK-1 Pathway Is Required for Resistance toPathogens (Basel, Switzerland) · 2022
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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

4 authors at 1 institution in 1 country.

Cheng-Gang ZouLaboratory for Conservation and Utilization of Bio-Resources, Yunnan University, Kunming, Yunnan 650091, China.
Yi-Cheng MaLaboratory for Conservation and Utilization of Bio-Resources, Yunnan University, Kunming, Yunnan 650091, China.
Li-Li DaiLaboratory for Conservation and Utilization of Bio-Resources, Yunnan University, Kunming, Yunnan 650091, China.
Ke-Qin ZhangLaboratory for Conservation and Utilization of Bio-Resources, Yunnan University, Kunming, Yunnan 650091, China kqzhang@ynu.edu.cn.
Yunnan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autophagy, a conserved pathway that delivers intracellular materials into lysosomes for degradation, is involved in development, aging, and a variety of diseases. Accumulating evidence demonstrates that autophagy plays a protective role against infectious diseases by diminishing intracellular pathogens, including bacteria, viruses, and parasites. However, the mechanism by which autophagy regulates innate immunity remains largely unknown. Here, we show that autophagy is involved in host defense against a pathogenic bacterium Pseudomonas aeruginosa in the metazoan Caenorhabditis elegans. P. aeruginosa infection induces autophagy via a conserved extracellular signal-regulated kinase (ERK). Intriguingly, impairment of autophagy does not influence the intestinal accumulation of P. aeruginosa, but instead induces intestinal necrosis. Inhibition of necrosis results in the survival of autophagy-deficient worms after P. aeruginosa infection. These findings reveal a previously unidentified role for autophagy in protection against necrosis triggered by pathogenic bacteria in C. elegans and implicate that such a function of autophagy may be conserved through the inflammatory response in diverse organisms.

Indexed as

AnimalsAutophagyCaenorhabditis elegansGene Knockdown TechniquesGenes, HelminthHost-Pathogen InteractionsImmunity, InnateMAP Kinase Signaling SystemMutationNecrosisPseudomonas aeruginosaPseudomonas InfectionsRNA Interference

Identifiers

PMID25114220
PMCPMC4151725
OpenAlexW2003699495

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.