Evidence map›Paper›PMID 29677174›Full record

ArticleMedical science monitor : international medical journal of experimental and clinical research2018

The Role of Autophagy and the Chemokine (C-X-C Motif) Ligand 16 During Acute Lung Injury in Mice.

Ye Gao, Ni Wang, Rui H Li, Yang Z Xiao

Open access · hybridAbstract read
In one paragraph

Article in Medical science monitor : international medical journal of experimental and clinical research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.6field-weighted citation impact, top 30% 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

7 citing papers in PubMed, 9 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Autophagy Induced by BCL2-Related ceRNA Network Participates in the Occurrence of COPD.International journal of chronic obstructive pulmonary disease · 2022
    Article
  5. Article
  6. Article
  7. Autophagy and pulmonary disease.Therapeutic advances in respiratory disease
    Review
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 2 institutions in 1 country.

Ye GaoDepartment of Emergency Anesthesia, Second Affiliated Hospital of Dalian Medical University, Dalian, Liaoning, China (mainland).
Ni WangDepartment of Emergency Anesthesia, Second Affiliated Hospital of Dalian Medical University, Dalian, Liaoning, China (mainland).
Rui H LiDepartment of Emergency Anesthesia, Second Affiliated Hospital of Dalian Medical University, Dalian, Liaoning, China (mainland).
Yang Z XiaoDepartment of Emergency Anesthesia, Second Affiliated Hospital of Dalian Medical University, Dalian, Liaoning, China (mainland).
Second Affiliated Hospital of Dalian Medical University · CNDalian Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND Acute lung injury (ALI) is responsible for mortality in hospitalized patients. Autophagy can negatively regulate inflammatory response, and CXCL16 (chemokine (C-X-C motif) ligand 16) is a kind of chemokine, which is closely related to the inflammatory response. However, the relationship between autophagy and CXCL16 in ALI is still unclear. This study aimed to investigate the role of autophagy and chemokine CXCL16 in ALI in mice. MATERIAL AND METHODS Thirty-two male C57BL/6 mice were divided into four groups. The control group (C group) was given normal saline through intraperitoneal injection. The L group was given LPS (lipopolysaccharide) at 30 mg/kg to construct an ALI model. The 3-MA group received an intraperitoneal injection of inhibitor of autophagy 3-methyladenine at 15 mg/kg, 30 minutes before LPS injection. The anti-CXCL16 group was given 20 mg/kg of CXCL16 monoclonal antibody 30 minutes before the LPS injection. RESULTS In the 3-MA Group, the level of histological analysis, lung wet/dry ratio, total protein of BAL (bronchoalveolar lavage fluid) and TNF-a level were higher than the L group (p<0.05), the level of autophagy was lower than the L group (p<0.05), and the level of CXCL16 was higher than the L group (p<0.05). In the anti-CXCL16 group, the level of histological analysis, lung wet/dry ratio, BAL protein, and TNF-α level were declined compared to the L group (p<0.05), but there was no statistically significant difference in expression of CXCL16 detected by ELISA between the anti-CXCL16 group and the L group (p>0.05). CONCLUSIONS Autophagy played a protective role in ALI induced by LPS in mice. Autophagy could regulate the level of CXCL16. The chemokine CXCL16 could exacerbate ALI.

Indexed as

Acute Lung InjuryAnimalsAutophagyBronchoalveolar Lavage FluidChemokine CXCL16Chemokines, CXCDisease Models, AnimalLigandsLipopolysaccharidesLungMaleMiceMice, Inbred C57BLTumor Necrosis Factor-alphaChemokine CXCL16Chemokines, CXCLigandsLipopolysaccharidesTumor Necrosis Factor-alpha

Identifiers

PMID29677174
PMCPMC5928852
OpenAlexW2799683169

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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 Socratic graph.