Evidence map›Paper›PMID 26264443›Full record

ArticleExperimental biology and medicine (Maywood, N.J.)2016

Phosphatase and tensin homolog deleted on chromosome 10 contributes to phenotype transformation of fibroblasts in idiopathic pulmonary fibrosis via multiple pathways.

Jing Geng, Xiaoxi Huang, Ying Li, Xuefeng Xu, Shuhong Li, Dingyuan Jiang, Zheng Liu, Huaping Dai

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Experimental biology and medicine (Maywood, N.J.), 2016. 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
1.2field-weighted citation impact, top 19% 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, 17 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 3 institutions in 1 country.

Jing GengDepartment of Respiratory and Critical Care Medicine, Beijing Key Laboratory of Respiratory and Pulmonary Circulation Disorders, Beijing Chao-Yang Hospital-Beijing Institute of Respiratory Medicine, Capital Medical University, Beijing 100020, P.R. China.
Xiaoxi HuangDepartment of Medical Research, Beijing Chao-Yang Hospital, Capital Medical University, Beijing 100020, P.R. China.
Ying LiDepartment of Medical Research, Beijing Chao-Yang Hospital, Capital Medical University, Beijing 100020, P.R. China.
Xuefeng XuDepartment of Respiratory and Critical Care Medicine, Beijing Key Laboratory of Respiratory and Pulmonary Circulation Disorders, Beijing Chao-Yang Hospital-Beijing Institute of Respiratory Medicine, Capital Medical University, Beijing 100020, P.R. China National Clinical Research Centre for Respiratory Medicine, Beijing Hospital, Beijing 100730, P.R. China.
Shuhong LiDepartment of Respiratory and Critical Care Medicine, Beijing Key Laboratory of Respiratory and Pulmonary Circulation Disorders, Beijing Chao-Yang Hospital-Beijing Institute of Respiratory Medicine, Capital Medical University, Beijing 100020, P.R. China.
Dingyuan JiangDepartment of Respiratory and Critical Care Medicine, Beijing Key Laboratory of Respiratory and Pulmonary Circulation Disorders, Beijing Chao-Yang Hospital-Beijing Institute of Respiratory Medicine, Capital Medical University, Beijing 100020, P.R. China.
Zheng LiuDepartment of Medical Research, Beijing Chao-Yang Hospital, Capital Medical University, Beijing 100020, P.R. China.
Huaping DaiDepartment of Respiratory and Critical Care Medicine, Beijing Key Laboratory of Respiratory and Pulmonary Circulation Disorders, Beijing Chao-Yang Hospital-Beijing Institute of Respiratory Medicine, Capital Medical University, Beijing 100020, P.R. China daihuaping@ccmu.edu.cn.
Beijing Chao-Yang Hospital · CNCapital Medical University · CNBeijing Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Idiopathic pulmonary fibrosis (IPF) is a progressive and fatal disease and considered as a cancer-like disease. The phosphatase and tensin homologue deleted on chromosome 10 (PTEN) tumor suppressor has drawn attention in the pathogenesis of IPF. However, the role of PTEN in phenotypic transformation of lung fibroblasts, particularly in the migratory and invasive phenotype, is still elusive. Our data showed that PTEN expression was markedly reduced in both fibroblasts and myofibroblasts from IPF patients. Furthermore, loss of PTEN led to the transformation of normal fibroblasts to myofibroblasts and increased proliferation, apoptosis resistance, and migration/invasion activities. PTEN deficiency upregulated hyaluronan synthase 2 expression and thereby enhanced the invasion ability of fibroblasts. Cross-talk between PTEN and the transforming growth factor β1 (TGF-β1) pathway and PTEN reduction by hypoxia were observed. These findings suggest that PTEN is implicated in multiple pathways and plays a crucial role in the pathogenesis of IPF.

Indexed as

Cell Transformation, NeoplasticAdultCell MovementCell ProliferationFibroblastsGlucuronosyltransferaseHumansHyaluronan SynthasesIdiopathic Pulmonary FibrosisLungMaleMiddle AgedPTEN PhosphohydrolaseTransforming Growth Factor beta1GlucuronosyltransferaseHAS2 protein, humanHyaluronan SynthasesPTEN PhosphohydrolasePTEN protein, humanTransforming Growth Factor beta1Fibroblastsidiopathic pulmonary fibrosisphenotype transformationphosphatase and tensin homologue deleted on chromosome 10

Identifiers

PMID26264443
PMCPMC4935394
OpenAlexW2298431271

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.