Evidence map›Paper›PMID 34036384›Full record

ArticleMolecular medicine reports2021

Endoplasmic reticulum stress promotes epithelial‑mesenchymal transition via the PERK signaling pathway in paraquat‑induced pulmonary fibrosis.

Xiaoxiao Meng, Kan Liu, Hui Xie, Yong Zhu, Wei Jin, Jian Lu, Ruilan Wang

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2021. 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
1.9field-weighted citation impact, top 15% 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, 14 citations in OpenAlex.

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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

7 authors at 2 institutions in 1 country.

Xiaoxiao Meng *Department of Critical Care Medicine, Shanghai General Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai 201620, P.R. China.
Kan Liu *Department of Diving Medicine, Faculty of Nautical Medicine, Second Military Medical University, Shanghai 200082, P.R. China.
Hui XieDepartment of Critical Care Medicine, Shanghai General Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai 201620, P.R. China.
Yong ZhuDepartment of Critical Care Medicine, Shanghai General Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai 201620, P.R. China.
Wei JinDepartment of Critical Care Medicine, Shanghai General Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai 201620, P.R. China.
Jian LuDepartment of Critical Care Medicine, Shanghai General Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai 201620, P.R. China.
Ruilan WangDepartment of Critical Care Medicine, Shanghai General Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai 201620, P.R. China.
Shanghai First People's Hospital · CNSecond Military Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pulmonary fibrosis is the primary reason for mortality in patients with paraquat (PQ) poisoning. Our previous study demonstrated that epithelial‑mesenchymal transition (EMT) had a role in PQ‑induced pulmonary fibrosis. However, the role of endoplasmic reticulum (ER) stress in PQ‑induced EMT remains clear. The present study aimed to determine the role of ER stress in EMT in PQ‑induced pulmonary fibrosis. A549 and RLE‑6TN cells were incubated with LY294002 (a PI3K inhibitor) or transfected with protein kinase RNA‑like ER kinase (PERK) small interfering RNA (si) for 24 h prior to being exposed to PQ. Next, the expression levels of ER stress‑related proteins, PI3K/AKT/GSK‑3β signaling pathway‑related proteins and EMT‑related markers were analyzed by performing western blotting, reverse transcription‑quantitative PCR and immunofluorescence assays. The results of the present study revealed that the protein expression levels of PERK, phosphorylated (p)‑PERK, p‑eukaryotic initiation factor 2 (eIF2)α were significantly upregulated in the PQ group, whereas p‑PI3K, p‑AKT and p‑GSK‑3β were significantly upregulated in the sicontrol + PQ group compared with the sicontrol group.

Indexed as

Alveolar Epithelial CellsAnimalsCell LineChromoneseIF-2 KinaseEndoplasmic Reticulum StressEpithelial-Mesenchymal TransitionEukaryotic Initiation Factor-2Gene Knockdown TechniquesGlycogen Synthase Kinase 3 betaHumansMorpholinesParaquatPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsProto-Oncogene Proteins c-akt2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-oneChromonesEIF2AK3 protein, humaneIF-2 KinaseEukaryotic Initiation Factor-2Glycogen Synthase Kinase 3 betaMorpholinesParaquatPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsProto-Oncogene Proteins c-aktendoplasmic reticulum stressepithelial‑mesenchymal transitionparaquatpulmonary fibrosis

Identifiers

PMID34036384
PMCPMC8170262
OpenAlexW3164687281

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.