Evidence map›Paper›PMID 29956395›Full record

ArticleCell proliferation2018

Concurrence of autophagy with apoptosis in alveolar epithelial cells contributes to chronic pulmonary toxicity induced by methamphetamine.

Yun Wang, Yu-Han Gu, Li-Ye Liang, Ming Liu, Bin Jiang, Mei-Jia Zhu, Xin Wang, Lin Shi

Open access · bronzeAbstract read
In one paragraph

Article in Cell proliferation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

13 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Substances of abuse and their effect on SAR-CoV-2 pathogenesis.NeuroImmune pharmacology and therapeutics · 2023
    Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
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

8 authors at 3 institutions in 1 country.

Yun WangDepartment of Clinical Pharmacology, School of Pharmacy, China Medical University, Shenyang, China.ORCID http://orcid.org/0000-0001-7146-8290
Yu-Han GuDepartment of Clinical Pharmacology, School of Pharmacy, China Medical University, Shenyang, China.
Li-Ye LiangDepartment of Clinical Pharmacology, School of Pharmacy, China Medical University, Shenyang, China.
Ming LiuDepartment of Drug Control, China Criminal Police University, Shenyang, China.
Bin JiangDepartment of Cardiovascular Ultrasound, The First Hospital, China Medical University, Shenyang, China.
Mei-Jia ZhuDepartment of Clinical Pharmacology, School of Pharmacy, China Medical University, Shenyang, China.
Xin WangDepartment of Clinical Pharmacology, School of Pharmacy, China Medical University, Shenyang, China.
Lin ShiDepartment of Clinical Pharmacology, School of Pharmacy, China Medical University, Shenyang, China.
China Medical University · CNCriminal Investigation Police University of China · CNFirst Hospital of China Medical University · CN

Funding

National Natural Science Foundation of China 81503058Natural Science Foundation of Liaoning Province 2014021065
6 · The paper itself

Abstract

objectivesMethamphetamine (MA) abuse evokes pulmonary toxicity. The aim of our study is to investigate if autophagy is induced by MA and if autophagy-initiated apoptosis in alveolar epithelial cells is involved in MA-induced chronic pulmonary toxicity. MATERIALS AND

methodsThe rats in Control group and MA group were tested by Doppler and HE staining. The alveolar epithelial cells were treated with MA, following by western blot, RT-PCR and immunofluorescence assay.

resultsChronic exposure to MA resulted in lower growth ratio of weight and in higher heart rate and peak blood flow velocity of the main pulmonary artery of rats. MA induced infiltration of inflammatory cells in lungs, more compact lung parenchyma, thickened alveolar septum and reduction in the number of alveolar sacs. In alveolar epithelial cells, the autophagy marker LC3 and per cent of cells containing LC3-positive autophagosome were significantly increased. MA dose dependently suppressed the phosphorylation of mTOR to inactivate mTOR, elicited autophagy regulatory proteins LC3 and Beclin-1, accelerated the transformation from LC3 I to LC3 II and initiated apoptosis by decreasing Bcl-2 and increasing Bax, Bax/Bcl-2 and cleaved Caspase 3. The above results suggest that sustained autophagy was induced by long-term exposure to MA and that the increased Beclin-1 autophagy initiated apoptosis in alveolar epithelial cells.

conclusionsConcurrence of autophagy with apoptosis in alveolar epithelial cells contributes to chronic pulmonary toxicity induced by MA.

Indexed as

A549 CellsAlveolar Epithelial CellsAnimalsApoptosisAutophagybcl-2-Associated X ProteinBeclin-1Caspase 3Cell Line, TumorHumansLungMaleMethamphetamineMicrotubule-Associated ProteinsPneumoniaRatsbcl-2-Associated X ProteinBeclin-1Caspase 3MethamphetamineMicrotubule-Associated Proteinsapoptosisautophagyaveolar epithelial cellsBeclin-1LC3methamphetamine

Identifiers

PMID29956395
PMCPMC6528941
OpenAlexW2810254864

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.