Evidence map›Paper›PMID 29673286›Full record

ArticleInnate immunity2018

Inhibition of autophagy with 3-methyladenine is protective in a lethal model of murine endotoxemia and polymicrobial sepsis.

Qirui Li, Lingyun Li, Xiaoyuan Fei, Yuanyue Zhang, Chang Qi, Shuyao Hua, Feili Gong, Min Fang

Open access · hybridAbstract read
In one paragraph

Article in Innate immunity, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

24 citing papers in PubMed, 52 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Sympathetic regulation of the host immune response to bacterial sepsis.Clinical science (London, England : 1979) · 2025
    Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. 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

8 authors at 1 institution in 1 country.

Qirui LiDepartment of Immunology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, China.
Lingyun LiDepartment of Immunology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, China.
Xiaoyuan FeiDepartment of Immunology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, China.
Yuanyue ZhangDepartment of Immunology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, China.
Chang QiDepartment of Immunology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, China.
Shuyao HuaDepartment of Immunology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, China.
Feili GongDepartment of Immunology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, China.
Min FangDepartment of Immunology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, China.ORCID 0000-0002-1835-5702
Huazhong University of Science and Technology · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Here, the regulatory role of autophagy is examined in both an LPS-induced lethal endotoxic shock mouse model and cecal ligation and puncture (CLP) mouse model. Autophagy-inhibitor 3-methyladenine (3-MA) and autophagy-enhancer rapamycin were administrated to mice challenged with LPS or CLP. Animals challenged with LPS or CLP combined with 3-MA displayed increased survival after endotoxemia, but LPS combined with rapamycin worsened the endotoxic shock of the mice. Among the different organs studied, the lungs and intestines exhibited significant differences among LPS alone, LPS combined with 3-MA and LPS combined with rapamycin. LPS combined with 3-MA attenuated the inflammatory damages of these organs as compared with LPS alone. In contrast, LPS combined with rapamycin increased damage in these organs. Consistently, serum inflammatory mediators TNF-α and IL-6 were decreased by the treatment of LPS combined with 3-MA as compared with LPS alone, while administration of LPS combined with rapamycin increased the serum TNF-α and IL-6 levels. Similar results were found in mouse bone marrow-derived macrophages exposed to LPS. Moreover, the regulatory effect of autophagy to endotoxic shock is dependent on the TLR4 signaling pathway. Our results demonstrate the central role of autophagy in the regulation of endotoxic shock and its potential modulation for endotoxic shock treatment.

Indexed as

AdenineAnimalsAutophagyCarrier ProteinsEndotoxemiaInterleukin-6LipopolysaccharidesMaleMiceMice, Inbred C57BLMicrotubule-Associated ProteinsSepsisShock, SepticSignal TransductionSirolimusTumor Necrosis Factor-alpha3-methyladenineAdenineCarrier ProteinsInterleukin-6LipopolysaccharidesMap1lc3b protein, mouseMicrotubule-Associated ProteinsSirolimusTLR4-associated protein, mouseTumor Necrosis Factor-alpha3-methyladenineAutophagyendotoxic shockrapamycinTLR4

Identifiers

PMID29673286
PMCPMC6830927
OpenAlexW2802404708

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.