Evidence map›Paper›PMID 26553601›Full record

ArticleAutophagy2015

Lipopolysaccharides may aggravate apoptosis through accumulation of autophagosomes in alveolar macrophages of human silicosis.

Shi Chen, Juxiang Yuan, Sanqiao Yao, Yulan Jin, Gang Chen, Wei Tian, Jinkun Xi, Zhelong Xu, Dong Weng, Jie Chen

Abstract read
In one paragraph

Article in Autophagy, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
5.5field-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

55 citing papers in PubMed, 107 citations in OpenAlex.

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  2. The Gut Microbiome and Metabolomics Profiles of Dust-exposed Rats.Combinatorial chemistry & high throughput screening · 2026
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  10. miR-29a-3p Regulates Autophagy by Targeting Akt3-Mediated mTOR in SiOInternational journal of molecular sciences · 2023
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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

10 authors at 5 institutions in 2 countries.

Shi Chena School of Public Health; China Medical University ; Shenyang , China.
Juxiang Yuanb School of Public Health; North China University of Science and Technology ; Tangshan , China.
Sanqiao Yaoc School of Public Health; Xinxiang Medical University ; Xinxiang , China.
Yulan Jinb School of Public Health; North China University of Science and Technology ; Tangshan , China.
Gang Chend Department of Pneumoconiosis ; Beidaihe Sanitarium for China Coal Miners ; Beidaihe , China.
Wei Tiane Heart Institute; North China University of Science and Technology ; Tangshan , China.
Jinkun Xie Heart Institute; North China University of Science and Technology ; Tangshan , China.
Zhelong Xue Heart Institute; North China University of Science and Technology ; Tangshan , China.
Dong Wenga School of Public Health; China Medical University ; Shenyang , China.
Jie Chena School of Public Health; China Medical University ; Shenyang , China.
North China University of Science and Technology · CNChina Medical University · CNBeihai People's Hospital · CNNational Heart Institute · MYXinxiang Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Silica dust mainly attacks alveolar macrophages (AMs) and increases the apoptosis of AMs in silicosis patients. However, it is still unclear whether autophagy is affected. Autophagy mainly has defensive functions in response to stress, contributing to cell survival in adverse conditions, and conversely it has also been implicated in cell death. Lipopolysaccharide (LPS) induces autophagy and apoptosis in macrophages. The role of LPS in autophagy and apoptosis in AMs of silicosis patients is unknown. In this study, we collected AMs from 53 male workers exposed to silica and divided them into an observer (control) group, and stage I, II and III patient groups. We found increased levels of LC3B, SQSTM1/p62 and BECN1,whereas the phosphorylation of MTOR,and levels of LAMP2, TLR4, MYD88, TICAM1, as well as the number of lysosomes decreased with the development of silicosis. LPS stimulation triggered autophagy and increased levels of SQSTM1 in AMs. The autophagy inhibitor, 3-methyladenine (3MA), inhibited LPS-induced apoptosis in the AMs of silicosis patients. Moreover, 3MA reversed the LPS-induced decrease in BCL2 and the increase in BAX and CASP3 levels in AMs. These results suggest that autophagosomes accumulate in AMs during silicosis progression. LPS can induce the formation of autophagosomes through a TLR4-dependent pathway, and LPS may exacerbate the apoptosis in AMs. Blockade of the formation of autophagosomes may inhibit LPS-induced apoptosis via the intrinsic apoptotic pathway in AMs. These findings describe novel mechanisms that may lead to new preventive and therapeutic strategies for pulmonary fibrosis.

Indexed as

ApoptosisApoptosis Regulatory ProteinsAutophagyCaspase 3Cell LineHumansLipopolysaccharidesLysosomesMacrophagesMacrophages, AlveolarSilicosisApoptosis Regulatory ProteinsCaspase 3Lipopolysaccharidesalveolar macrophagesapoptosisautophagic degradationautophagosomeautophagyLPSlysosomesilicosisTLR4

Identifiers

PMID26553601
PMCPMC4835201
OpenAlexW2099612743

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.