Evidence map›Paper›PMID 37875355›Full record

ArticleZhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences2023

Role of PI3K/Akt/mTOR pathway-mediated macrophage autophagy in affecting the phenotype transformation of lung fibroblasts induced by silica dust exposure.

Yue DU, Fangcai Huang, Lan Guan, Ming Zeng

Open access · greenAbstract read
In one paragraph

Article in Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.6field-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

8 citing papers in PubMed, 6 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

4 authors at 1 institution in 1 country.

Yue DUDepartment of Health Toxicology, Xiangya School of Public Health, Central South University, Changsha 410006, China. 216912054@csu.edu.cn.
Fangcai HuangDepartment of Health Toxicology, Xiangya School of Public Health, Central South University, Changsha 410006, China. lizuihfc@163.com.
Lan GuanDepartment of Health Toxicology, Xiangya School of Public Health, Central South University, Changsha 410006, China.
Ming ZengDepartment of Health Toxicology, Xiangya School of Public Health, Central South University, Changsha 410006, China. zengming@csu.edu.cn.
Central South University · CN

Funding

the National Natural Science Foundation of China 81673225
6 · The paper itself

Abstract

objectivesThe phosphoinositide 3-kinase/protein kinase B/mammalian target of rapamycin (PI3K/Akt/mTOR) pathway is one of the main signaling pathways related to autophagy. Autophagy plays a key role in the formation of silicosis fibrosis. The phenotypic transformation of lung fibroblasts into myofibroblasts is a hallmark of the transition from the inflammatory phase to the fibrotic phase in silicosis. This study aims to investigate whether the PI3K/Akt/mTOR pathway affects the phenotypic transformation of silicosis-induced lung fibroblasts into myofibroblasts via mediating macrophage autophagy.

methodsThe human monocytic leukemia cell line THP-1 cells were differentiated into macrophages by treating with 100 ng/mL of phorbol ester for 24 h. Macrophages were exposed to different concentrations (0, 25, 50, 100, 200, 400 μg/mL) and different times (0, 6, 12, 24, 48 h) of SiO

resultsAfter the macrophages were exposed to SiO

conclusionsSilica dust exposure inhibits the PI3K/Akt/mTOR pathway, increases autophagy and concentration of inflammatory factors in macrophages, and promotes the phenotype transformation of HFL-1 cells into myofibroblasts. The regulation of the PI3K/Akt/mTOR pathway can affect the autophagy induction and the concentration of inflammatory factors of macrophages by silica dust exposure, and then affect the phenotype transformation of HFL-1 cells into myofibroblasts induced by silica dust exposure.

Indexed as

Proto-Oncogene Proteins c-aktSilicosisAutophagyBeclin-1DustFibroblastsHumansLungMacrophagesMatrix Metalloproteinase 1Phosphatidylinositol 3-KinasesSilicon DioxideSirolimusTissue Inhibitor of Metalloproteinase-1TOR Serine-Threonine KinasesTransforming Growth Factor beta1Beclin-1DustMatrix Metalloproteinase 1Phosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSilicon DioxideSirolimusTissue Inhibitor of Metalloproteinase-1TOR Serine-Threonine KinasesTransforming Growth Factor beta1Tumor Necrosis Factor-alphalung fibroblastsmacrophage autophagymyofibroblastsphosphatidylinositol-3-kinase-protein kinase B-mammalian target of rapamycin pathwaysilica dusttransforming growth factor-β1tumor necrosis factor-α

Identifiers

PMID37875355
PMCPMC10930851
OpenAlexW4387930703

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.