Evidence map›Paper›PMID 32368013›Full record

ArticleDrug design, development and therapy2020

ACE2 Attenuates Epithelial-Mesenchymal Transition in MLE-12 Cells Induced by Silica.

Shumin Li, Yaqian Li, Hong Xu, Zhongqiu Wei, Yi Yang, Fuyu Jin, Min Zhang, Chen Wang, Wenxiong Song, Jingchen Huo and 3 more

Open access · goldAbstract read
In one paragraph

Article in Drug design, development and therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.5field-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

12 citing papers in PubMed, 25 citations in OpenAlex.

  1. Review
  2. Article
  3. Effect of macrophage-to-myofibroblast transition on silicosis.Animal models and experimental medicine · 2025
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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

13 authors at 1 institution in 1 country.

Shumin Li *School of Public Health, North China University of Science and Technology, Tangshan, Hebei 063210, People's Republic of China.ORCID 0000-0001-8083-1071
Yaqian Li *School of Basic Medical Sciences, North China University of Science and Technology, Tangshan, Hebei 063210, People's Republic of China.ORCID 0000-0001-9061-2665
Hong XuHebei Key Laboratory for Organ Fibrosis, North China University of Science and Technology, Tangshan, Hebei 063210, People's Republic of China.ORCID 0000-0002-3655-3833
Zhongqiu WeiSchool of Basic Medical Sciences, North China University of Science and Technology, Tangshan, Hebei 063210, People's Republic of China.
Yi YangAcademic Affairs Office, North China University of Science and Technology, Tangshan, Hebei 063210, People's Republic of China.
Fuyu JinSchool of Basic Medical Sciences, North China University of Science and Technology, Tangshan, Hebei 063210, People's Republic of China.ORCID 0000-0002-2855-9610
Min ZhangHebei Key Laboratory for Organ Fibrosis, North China University of Science and Technology, Tangshan, Hebei 063210, People's Republic of China.ORCID 0000-0002-6284-8272
Chen WangHebei Key Laboratory for Organ Fibrosis, North China University of Science and Technology, Tangshan, Hebei 063210, People's Republic of China.ORCID 0000-0001-8267-2932
Wenxiong SongSchool of Basic Medical Sciences, North China University of Science and Technology, Tangshan, Hebei 063210, People's Republic of China.ORCID 0000-0001-9893-5071
Jingchen HuoSchool of Basic Medical Sciences, North China University of Science and Technology, Tangshan, Hebei 063210, People's Republic of China.ORCID 0000-0002-8480-3665
Jingyuan ZhaoSchool of Basic Medical Sciences, North China University of Science and Technology, Tangshan, Hebei 063210, People's Republic of China.
Xiuhong YangSchool of Basic Medical Sciences, North China University of Science and Technology, Tangshan, Hebei 063210, People's Republic of China.
Fang YangSchool of Public Health, North China University of Science and Technology, Tangshan, Hebei 063210, People's Republic of China.ORCID 0000-0002-8783-8652
North China University of Science and Technology · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeThe role of angiotensin-converting enzyme 2 (ACE2) in silicosis remains unknown, although previous studies have suggested that ACE2 may be beneficial. We, therefore, investigated the effect of ACE2 on silicosis, particularly with regard to its role in regulating the epithelial-mesenchymal transition (EMT) induced by silica, with the aim to uncover a new potential target for the treatment of pulmonary fibrosis. MATERIALS AND

methodsWe employed wild-type mice treated with diminazene aceturate (DIZE, an ACE2 activator, 15 mg/kg/day for 4 weeks),

resultsDIZE treatment and overexpression of ACE2 markedly inhibited the formation of silica-induced lung fibrosis and increased the level of E-cadherin, with concomitant downregulation of pro-collagen, vimentin, and α-SMA via RAS signaling. Furthermore, DIZE and Ang-(1-7) attenuated the EMT and collagen deposition induced by silica in MLE-12 cells. Moreover, these effects were abrogated by MLN-4760 (a specific ACE2 inhibitor) and A779 (a specific Mas receptor blocker).

conclusionThe overexpression of

Indexed as

Angiotensin-Converting Enzyme 2AnimalsCell LineDose-Response Relationship, DrugEpithelial-Mesenchymal TransitionMaleMiceMice, Inbred ICRSilicon DioxideSilicosisStructure-Activity RelationshipAce2 protein, mouseAngiotensin-Converting Enzyme 2Silicon Dioxideangiotensin-converting enzymeangiotensin-converting enzyme 2diminazene aceturaterenin–angiotensin systemsilicosis fibrosistransgenic mice

Identifiers

PMID32368013
PMCPMC7183338
OpenAlexW3016458389

What OpenQuestion holds

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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.