Evidence map›Paper›PMID 31186017›Full record

ArticleRespiratory research2019

Piezo1 induced apoptosis of type II pneumocytes during ARDS.

Guo-Peng Liang, Jing Xu, Li-Li Cao, Yi-Hua Zeng, Bai-Xu Chen, Jing Yang, Zhong-Wei Zhang, Yan Kang

Open access · goldAbstract read
In one paragraph

Article in Respiratory research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

40 citing papers in PubMed, 56 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

8 authors at 2 institutions in 1 country.

Guo-Peng LiangDepartment of Critical Care Medicine, West China School of Medicine and West China Hospital, Sichuan University, Chengdu, 610041, China.
Jing XuDepartment of Critical Care Medicine, West China School of Medicine and West China Hospital, Sichuan University, Chengdu, 610041, China.
Li-Li CaoChengdu Medical College, Chengdu, 610041, Sichuan, China.
Yi-Hua ZengDepartment of Respiratory Critical Care Medicine, West China School of Medicine and West China Hospital, Sichuan University, Chengdu, 610041, China.
Bai-Xu ChenDepartment of Critical Care Medicine, West China School of Medicine and West China Hospital, Sichuan University, Chengdu, 610041, China.
Jing YangDepartment of Critical Care Medicine, West China School of Medicine and West China Hospital, Sichuan University, Chengdu, 610041, China.
Zhong-Wei ZhangDepartment of Critical Care Medicine, West China School of Medicine and West China Hospital, Sichuan University, Chengdu, 610041, China. 716461751@qq.com.
Yan KangDepartment of Critical Care Medicine, West China School of Medicine and West China Hospital, Sichuan University, Chengdu, 610041, China. kangyan@scu.edu.cn.
Sichuan University · CNChengdu Medical College · CN

Funding

Education Department of Sichuan Province 11ZA297National Natural Science Foundation of China 31301116Project of Sichuan Science and Technology 2019YFS0235
6 · The paper itself

Abstract

objectiveThe mechanisms of lung injury in acute respiratory distress syndrome (ARDS) are not well understood.Piezo1 was recently identified as a mechanotransduction protein. The present study found the expression of Piezo1 in type II pneumocytes and investigated its role in mediating ARDS-related lung injury.

methodsSprague-Dawley rats were used to establish an ARDS model, the expression of Piezo1,lung injuries, apoptosis as well as calcium influx were assessed.

resultsPiezo1 was expressed in type II pneumocytes as shown by immunofluorescence staining and expression was increased in the ARDS model. Knockdown of Piezo1 reduced apoptosis which was related to the elevation of Bcl-2.Calcium influx played a vital role in Piezo1-induced apoptosis.

conclusionPiezo1 was expressed in type II pneumocytes. Mechanical stretch of alveoli during ARDS induced activation of the Piezo1 channel,which resulted in calcium influx. The increased intracellular Ca2+ induced the apoptosis of type II pneumocytes, which may be related to the Bcl-2 pathway.

Indexed as

Stress, MechanicalA549 CellsAlveolar Epithelial CellsAnimalsApoptosisHumansIon ChannelsMembrane ProteinsRatsRats, Sprague-DawleyRespiratory Distress SyndromeIon ChannelsMembrane ProteinsPiezo1 protein, ratAcute respiratory distress syndromeLung injury;Piezo1;apoptosis;Ca2+

Identifiers

PMID31186017
PMCPMC6558715
OpenAlexW2951494953

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.