Evidence map›Paper›PMID 32715876›Full record

ArticleThe Journal of international medical research2020

The PI3K/AKT/mTOR pathway regulates autophagy to induce apoptosis of alveolar epithelial cells in chronic obstructive pulmonary disease caused by PM2.5 particulate matter.

Fang Zhang, Hui Ma, Zhong Lan Wang, Wei Hua Li, Hua Liu, Yan Xia Zhao

Open access · goldAbstract read
In one paragraph

Article in The Journal of international medical research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 1 pooled it
4.9field-weighted citation impact, top 4% 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

29 citing papers in PubMed, 1 synthesis or guideline pooled it, 57 citations in OpenAlex.

  1. Pooled it
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  19. The Effects and Pathogenesis of PM2.5 and Its Components on Chronic Obstructive Pulmonary Disease.International journal of chronic obstructive pulmonary disease · 2023
    Review
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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

6 authors at 1 institution in 1 country.

Fang ZhangDepartment of Respiration, Gansu Province People Hospital, Lanzhou City, Gansu Province, China.ORCID https://orcid.org/0000-0002-2615-2251
Hui MaDepartment of Respiratory, Gansu Province People Hospital, Lanzhou City, Gansu Province, China.
Zhong Lan WangDepartment of Respiratory Diseases, Gansu Province People Hospital, Lanzhou City, Gansu Province, China.
Wei Hua LiDepartment of Central Laboratory, Gansu Province People Hospital, Lanzhou City, Gansu Province, China.
Hua LiuDepartment of Respiration, Gansu Province People Hospital, Lanzhou City, Gansu Province, China.
Yan Xia ZhaoDepartment of Respiration, Gansu Province People Hospital, Lanzhou City, Gansu Province, China.
Gansu Provincial Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveMany lung diseases are associated with changes in autophagic activity. The phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) signaling pathway plays a key regulatory role in autophagy. Our aim was to explore the function of PI3K/AKT/mTOR pathway on autophagy in chronic obstructive pulmonary disease (COPD) caused by particulate matter with a diameter <2.5 µm (PM2.5).

methodsMale C57BL/6 mice were randomly divided into sham, model, and PI3K inhibitor groups. Mice were exposed to PM2.5 for 4 weeks to establish an

resultsIn mice with COPD induced by PM2.5, the PI3K inhibitor PF-04979064 suppressed protein expression of PI3K, p-AKT, and p-mTOR to increase apoptosis of alveolar epithelial cells and reduce autophagy. Short interfering PI3K suppressed the PI3K/AKT/mTOR pathway to induce apoptosis and reduce autophagy of alveolar epithelial cells in an

conclusionsThese data demonstrate that PI3K/AKT/mTOR pathway regulates autophagy to induce apoptosis of alveolar epithelial cells in COPD.

Indexed as

Proto-Oncogene Proteins c-aktPulmonary Disease, Chronic ObstructiveAlveolar Epithelial CellsAnimalsApoptosisAutophagyMaleMiceMice, Inbred C57BLParticulate MatterPhosphatidylinositol 3-KinasePhosphatidylinositol 3-KinasesTOR Serine-Threonine KinasesParticulate MatterPhosphatidylinositol 3-KinasePhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktTOR Serine-Threonine Kinasesalveolar epithelial cellsautophagyChronic obstructive pulmonary diseaselung diseaseparticulate matterPI3K/AKT/mTOR pathway

Identifiers

PMID32715876
PMCPMC7385846
OpenAlexW3043870092

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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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.