Evidence map›Paper›PMID 27658023›Full record

ArticleAutophagy2016

Activation of MTOR in pulmonary epithelium promotes LPS-induced acute lung injury.

Yue Hu, Jian Lou, Yuan-Yuan Mao, Tian-Wen Lai, Li-Yao Liu, Chen Zhu, Chao Zhang, Juan Liu, Yu-Yan Li, Fan Zhang and 4 more

Open access · bronzeAbstract read
In one paragraph

Article in Autophagy, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 111 papers.

0numbers the graph read from it
0cells of the map it votes in
111citing papers in PubMed
13.1field-weighted citation impact, top 1% 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

111 citing papers in PubMed, 201 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Polyploidy and Senescence of Cancer Cells: Impact of Cell Fusion.Advances in experimental medicine and biology · 2026
    Review
  8. Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article

51 more citing papers are in PubMed but not listed here.

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

14 authors at 1 institution in 1 country.

Yue Hua Department of Respiratory and Critical Care Medicine , Second Affiliated Hospital of Zhejiang University School of Medicine , Hangzhou , China.
Jian Loua Department of Respiratory and Critical Care Medicine , Second Affiliated Hospital of Zhejiang University School of Medicine , Hangzhou , China.
Yuan-Yuan Maoa Department of Respiratory and Critical Care Medicine , Second Affiliated Hospital of Zhejiang University School of Medicine , Hangzhou , China.
Tian-Wen Laia Department of Respiratory and Critical Care Medicine , Second Affiliated Hospital of Zhejiang University School of Medicine , Hangzhou , China.
Li-Yao Liua Department of Respiratory and Critical Care Medicine , Second Affiliated Hospital of Zhejiang University School of Medicine , Hangzhou , China.
Chen Zhua Department of Respiratory and Critical Care Medicine , Second Affiliated Hospital of Zhejiang University School of Medicine , Hangzhou , China.
Chao Zhanga Department of Respiratory and Critical Care Medicine , Second Affiliated Hospital of Zhejiang University School of Medicine , Hangzhou , China.
Juan Liua Department of Respiratory and Critical Care Medicine , Second Affiliated Hospital of Zhejiang University School of Medicine , Hangzhou , China.
Yu-Yan Lia Department of Respiratory and Critical Care Medicine , Second Affiliated Hospital of Zhejiang University School of Medicine , Hangzhou , China.
Fan Zhanga Department of Respiratory and Critical Care Medicine , Second Affiliated Hospital of Zhejiang University School of Medicine , Hangzhou , China.
Wen Lia Department of Respiratory and Critical Care Medicine , Second Affiliated Hospital of Zhejiang University School of Medicine , Hangzhou , China.
Song-Min Yinga Department of Respiratory and Critical Care Medicine , Second Affiliated Hospital of Zhejiang University School of Medicine , Hangzhou , China.
Zhi-Hua Chena Department of Respiratory and Critical Care Medicine , Second Affiliated Hospital of Zhejiang University School of Medicine , Hangzhou , China.
Hua-Hao Shena Department of Respiratory and Critical Care Medicine , Second Affiliated Hospital of Zhejiang University School of Medicine , Hangzhou , China.
Second Affiliated Hospital of Zhejiang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

MTOR (mechanistic target of rapamycin [serine/threonine kinase]) plays a crucial role in many major cellular processes including metabolism, proliferation and macroautophagy/autophagy induction, and is also implicated in a growing number of proliferative and metabolic diseases. Both MTOR and autophagy have been suggested to be involved in lung disorders, however, little is known about the role of MTOR and autophagy in pulmonary epithelium in the context of acute lung injury (ALI). In the present study, we observed that lipopolysaccharide (LPS) stimulation induced MTOR phosphorylation and decreased the expression of MAP1LC3B/LC3B (microtubule-associated protein 1 light chain 3 β)-II, a hallmark of autophagy, in mouse lung epithelium and in human bronchial epithelial (HBE) cells. The activation of MTOR in HBE cells was mediated by TLR4 (toll-like receptor 4) signaling. Genetic knockdown of MTOR or overexpression of autophagy-related proteins significantly attenuated, whereas inhibition of autophagy further augmented, LPS-induced expression of IL6 (interleukin 6) and IL8, through NFKB signaling in HBE cells. Mice with specific knockdown of Mtor in bronchial or alveolar epithelial cells exhibited significantly attenuated airway inflammation, barrier disruption, and lung edema, and displayed prolonged survival in response to LPS exposure. Taken together, our results demonstrate that activation of MTOR in the epithelium promotes LPS-induced ALI, likely through downregulation of autophagy and the subsequent activation of NFKB. Thus, inhibition of MTOR in pulmonary epithelial cells may represent a novel therapeutic strategy for preventing ALI induced by certain bacteria.

Indexed as

Acute Lung InjuryAnimalsAutophagyBronchiCell LineEnzyme ActivationEpithelial CellsEpitheliumGene Knockdown TechniquesHumansInflammationInflammation MediatorsLipopolysaccharidesLungMice, Inbred C57BLMicrotubule-Associated ProteinsInflammation MediatorsLipopolysaccharidesMap1lc3b protein, mouseMicrotubule-Associated ProteinsNF-kappa BSirolimusToll-Like Receptor 4TOR Serine-Threonine Kinasesacute lung injuryautophagyepitheliuminflammationMTOR

Identifiers

PMID27658023
PMCPMC5173285
OpenAlexW2523712370

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.