Evidence map›Paper›PMID 30484494›Full record

ArticleBrazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica2018

YAP activation promotes the transdifferentiation of cardiac fibroblasts to myofibroblasts in matrix remodeling of dilated cardiomyopathy.

Bo Jin, Jun Zhu, Hai-Ming Shi, Zhi-Chao Wen, Bang-Wei Wu

Open access · goldAbstract read
In one paragraph

Article in Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.2field-weighted citation impact, top 23% 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

14 citing papers in PubMed, 22 citations in OpenAlex.

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  8. Effect of Inactivation ofJournal of the Endocrine Society · 2022
    Article
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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

5 authors at 2 institutions in 1 country.

Bo JinDepartment of Cardiology, Huashan Hospital, Fudan University, Shanghai, China.
Jun ZhuDepartment of Cardiology, Huashan Hospital, Fudan University, Shanghai, China.
Hai-Ming ShiDepartment of Cardiology, Huashan Hospital, Fudan University, Shanghai, China.
Zhi-Chao WenDepartment of Cardiology, Huashan Hospital, Fudan University, Shanghai, China.
Bang-Wei WuDepartment of Cardiology, Huashan Hospital, Fudan University, Shanghai, China.
Fudan University · CNHuashan Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Yes-associated protein (YAP) is an important regulator of cellular proliferation and transdifferentiation. However, little is known about the mechanisms underlying myofibroblast transdifferentiation in dilated cardiomyopathy (DCM). We investigated the role of YAP in the pathological process of cardiac matrix remodeling. A classic model of DCM was established in BALB/c mice by immunization with porcine cardiac myosin. Cardiac fibroblasts were isolated from neonatal Sprague-Dawley rats by density gradient centrifugation. The expression levels of α-smooth muscle actin (α-SMA) and collagen volume fraction (CVF) were significantly increased in DCM mice. Angiotensin II (Ang II)-mediated YAP activation promoted the proliferation and transdifferentiation of neonatal rat cardiac fibroblasts, and this effect was significantly suppressed in the shRNA YAP + Ang II group compared with the shRNA Control + Ang II group in vitro (2.98±0.34 ×105 vs 5.52±0.82 ×105, P<0.01). Inhibition of endogenous Ang II-stimulated YAP improved the cardiac function by targeting myofibroblast transdifferentiation to attenuate matrix remodeling in vivo. In the valsartan group, left ventricular ejection fraction and fractional shortening were significantly increased compared with the DCM group (52.72±5.51% vs 44.46±3.01%, P<0.05; 34.84±3.85% vs 26.65±3.12%, P<0.01). Our study demonstrated that YAP was a regulator of cardiac myofibroblast differentiation, and regulation of YAP signaling pathway contributed to improve cardiac function of DCM mice, possibly in part by decreasing myofibroblast transdifferentiation to inhibit matrix remodeling.

Indexed as

Adaptor Proteins, Signal TransducingAngiotensin IIAnimalsBlotting, WesternCardiomyopathy, DilatedCell Cycle ProteinsCell DifferentiationCell TransdifferentiationDisease Models, AnimalEchocardiographyMaleMiceMice, Inbred BALB CMicroscopy, FluorescenceMyofibroblastsPhosphoproteinsAdaptor Proteins, Signal TransducingAngiotensin IICell Cycle ProteinsPhosphoproteinsYap1 protein, mouseYAP-Signaling Proteins

Identifiers

PMID30484494
PMCPMC6262745
OpenAlexW2901491632

What OpenQuestion 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 OpenQuestion graph.