Evidence map›Paper›PMID 30644438›Full record

ArticleCell death and differentiation2019

YAP1/Twist promotes fibroblast activation and lung fibrosis that conferred by miR-15a loss in IPF.

Yingzhun Chen, Xiaoguang Zhao, Jian Sun, Wei Su, Lu Zhang, Yingnan Li, Yingqi Liu, Lijia Zhang, Yanjie Lu, Hongli Shan and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Cell death and differentiation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed, 3 pooled it
4.8field-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

64 citing papers in PubMed, 3 syntheses or guidelines pooled it, 97 citations in OpenAlex.

  1. Pooled it
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  11. Mechanosensing Pathways in the Progression of Pulmonary Fibrosis.Current opinion in biomedical engineering · 2025
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4 more citing papers are in PubMed but not listed here.

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

11 authors at 2 institutions in 1 country.

Yingzhun ChenDepartment of Pharmacology (State-Province Key Laboratories of Biomedicine-Pharmaceutics of China, Key Laboratory of Cardiovascular Research, Ministry of Education), College of Pharmacy, Harbin Medical University, Harbin, Heilongjiang, 150081, People's Republic of China.
Xiaoguang ZhaoDepartment of Pharmacology (State-Province Key Laboratories of Biomedicine-Pharmaceutics of China, Key Laboratory of Cardiovascular Research, Ministry of Education), College of Pharmacy, Harbin Medical University, Harbin, Heilongjiang, 150081, People's Republic of China.
Jian SunDepartment of Pharmacology (State-Province Key Laboratories of Biomedicine-Pharmaceutics of China, Key Laboratory of Cardiovascular Research, Ministry of Education), College of Pharmacy, Harbin Medical University, Harbin, Heilongjiang, 150081, People's Republic of China.
Wei SuDepartment of Pharmacology (State-Province Key Laboratories of Biomedicine-Pharmaceutics of China, Key Laboratory of Cardiovascular Research, Ministry of Education), College of Pharmacy, Harbin Medical University, Harbin, Heilongjiang, 150081, People's Republic of China.
Lu ZhangDepartment of Pharmacology (State-Province Key Laboratories of Biomedicine-Pharmaceutics of China, Key Laboratory of Cardiovascular Research, Ministry of Education), College of Pharmacy, Harbin Medical University, Harbin, Heilongjiang, 150081, People's Republic of China.
Yingnan LiDepartment of Pharmacology (State-Province Key Laboratories of Biomedicine-Pharmaceutics of China, Key Laboratory of Cardiovascular Research, Ministry of Education), College of Pharmacy, Harbin Medical University, Harbin, Heilongjiang, 150081, People's Republic of China.
Yingqi LiuDepartment of Pharmacology (State-Province Key Laboratories of Biomedicine-Pharmaceutics of China, Key Laboratory of Cardiovascular Research, Ministry of Education), College of Pharmacy, Harbin Medical University, Harbin, Heilongjiang, 150081, People's Republic of China.
Lijia ZhangDepartment of Pharmacology (State-Province Key Laboratories of Biomedicine-Pharmaceutics of China, Key Laboratory of Cardiovascular Research, Ministry of Education), College of Pharmacy, Harbin Medical University, Harbin, Heilongjiang, 150081, People's Republic of China.
Yanjie LuDepartment of Pharmacology (State-Province Key Laboratories of Biomedicine-Pharmaceutics of China, Key Laboratory of Cardiovascular Research, Ministry of Education), College of Pharmacy, Harbin Medical University, Harbin, Heilongjiang, 150081, People's Republic of China.
Hongli ShanDepartment of Pharmacology (State-Province Key Laboratories of Biomedicine-Pharmaceutics of China, Key Laboratory of Cardiovascular Research, Ministry of Education), College of Pharmacy, Harbin Medical University, Harbin, Heilongjiang, 150081, People's Republic of China.
Haihai LiangDepartment of Pharmacology (State-Province Key Laboratories of Biomedicine-Pharmaceutics of China, Key Laboratory of Cardiovascular Research, Ministry of Education), College of Pharmacy, Harbin Medical University, Harbin, Heilongjiang, 150081, People's Republic of China. lianghaihai@ems.hrbmu.edu.cn.
Harbin Medical University · CNHeilongjiang Academy of Sciences · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive, fibrotic parenchymal lung disease of unknown etiology and lack effective interventions. Using a combination of in vitro and in vivo studies, we found that overexpression of YAP1, a key effector in the Hippo pathway, promoted cell proliferation, migration, and collagen production in lung fibroblasts. Furthermore, the pro-fibrotic action of YAP1 was mediated by transcriptional activation of Twist1 through interacting with its partner TEAD. In contrast, knockdown of YAP1 inhibited extracellular matrix (ECM) deposition, which ultimately ameliorated lung fibrosis in vitro and in vivo. Additionally, we constructed a dysregulated miRNA regulatory network that affects the expression of the Hippo pathway effectors in IPF and identified miR-15a, which is significantly down-regulated in IPF patients, as one of the most essential miRNAs regulating this pathway. Moreover, knockdown of miR-15a resulted in fibroblast activation and lung fibrosis through promoting Twist expression by targeting inhibition of YAP1. In contrast, therapeutic restoration of miR-15a inhibits fibrogenesis in lung fibroblast and abrogated BLM-induced lung fibrosis in mice. These results highlight a role for miR-15a/YAP1/Twist axis in IPF that offer novel strategies for the prevention and treatment of lung fibrosis.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsBleomycinCell Cycle ProteinsCell DifferentiationCell ProliferationDatabases, Nucleic AcidDisease Models, AnimalExtracellular MatrixFibroblastsFibrosisHumansIdiopathic Pulmonary FibrosisLungMiceMice, Inbred C57BLAdaptor Proteins, Signal TransducingBleomycinCell Cycle ProteinsMicroRNAsMirn15a microRNA, mouseMIRN15 microRNA, humanRNA, Small InterferingTranscription FactorsTransforming Growth Factor beta1Twist-Related Protein 1YAP1 protein, humanYap1 protein, mouseYAP-Signaling Proteins

Identifiers

PMID30644438
PMCPMC6748107
OpenAlexW2910874028

What OpenQuestion holds

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Read underepoch 390

Registered trials

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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.