Evidence map›Paper›PMID 36864465›Full record

ArticleCell & bioscience2023

Activation of the Hedgehog signaling pathway leads to fibrosis in aortic valves.

Dongsheng Gu, Arvin H Soepriatna, Wenjun Zhang, Jun Li, Jenny Zhao, Xiaoli Zhang, Xianhong Shu, Yongshi Wang, Benjamin J Landis, Craig J Goergen and 1 more

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

Article in Cell & bioscience, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.9field-weighted citation impact, top 26% 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

1 citing paper in PubMed, 6 citations in OpenAlex.

  1. Article
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 5 institutions in 2 countries.

Dongsheng Gu *Department of Pediatrics, Indiana University School of Medicine, Wells Center for Pediatric Research, 1040 W. Walnut Street., Indianapolis, IN, 46202, USA.
Arvin H Soepriatna *Purdue University Weldon School of Biomedical Engineering, 206 S. Martin Jischke Drive, Room 3025, West Lafayette, IN, 47907, USA.
Wenjun ZhangDepartment of Pediatrics, Indiana University School of Medicine, Wells Center for Pediatric Research, 1040 W. Walnut Street., Indianapolis, IN, 46202, USA.
Jun LiShanghai Institute of Cardiovascular Diseases, Zhongshan Hospital Fudan University, 180 Fenglin Road, Shanghai, 200032, China.
Jenny ZhaoDepartment of Pediatrics, Indiana University School of Medicine, Wells Center for Pediatric Research, 1040 W. Walnut Street., Indianapolis, IN, 46202, USA.
Xiaoli ZhangDepartment of Pediatrics, Indiana University School of Medicine, Wells Center for Pediatric Research, 1040 W. Walnut Street., Indianapolis, IN, 46202, USA.
Xianhong ShuShanghai Institute of Cardiovascular Diseases, Zhongshan Hospital Fudan University, 180 Fenglin Road, Shanghai, 200032, China.
Yongshi WangShanghai Institute of Cardiovascular Diseases, Zhongshan Hospital Fudan University, 180 Fenglin Road, Shanghai, 200032, China. wang.yongshi@zs-hospital.sh.cn.
Benjamin J LandisDepartment of Pediatrics, Indiana University School of Medicine, Wells Center for Pediatric Research, 1040 W. Walnut Street., Indianapolis, IN, 46202, USA. benjland@iu.edu.
Craig J GoergenPurdue University Weldon School of Biomedical Engineering, 206 S. Martin Jischke Drive, Room 3025, West Lafayette, IN, 47907, USA. cgoergen@purdue.edu.
Jingwu XieDepartment of Pediatrics, Indiana University School of Medicine, Wells Center for Pediatric Research, 1040 W. Walnut Street., Indianapolis, IN, 46202, USA. jwx19631019@gmail.com.ORCID http://orcid.org/0000-0002-3674-332X
Indiana University School of MedicineSun Yat-sen University · CNPurdue University West Lafayette · USBoston University · USNational Institutes of Health · US

Funding

Investigating the role of mitochondria in thoracic aortic aneurysm pathogenesisK23HL141667 · NHLBI · INDIANA UNIVERSITY INDIANAPOLIS · PI LANDIS, BENJAMIN JOHN · 2019 to 2023
$810k
NHLBI NIH HHS K23 HL141667NHLBI NIH HHS L30 HL138894
6 · The paper itself

Abstract

backgroundFibrosis is a pathological wound healing process characterized by excessive extracellular matrix deposition, which interferes with normal organ function and contributes to ~ 45% of human mortality. Fibrosis develops in response to chronic injury in nearly all organs, but the a cascade of events leading to fibrosis remains unclear. While hedgehog (Hh) signaling activation has been associated with fibrosis in the lung, kidney, and skin, it is unknown whether hedgehog signaling activation is the cause or the consequence of fibrosis. We hypothesize that activation of hedgehog signaling is sufficient to drive fibrosis in mouse models.

resultsIn this study, we provide direct evidence to show that activation of Hh signaling via expression of activated smoothened, SmoM2, is sufficient to induce fibrosis in the vasculature and aortic valves. We showed that activated SmoM2 -induced fibrosis is associated with abnormal function of aortic valves and heart. The relevance of this mouse model to human health is reflected in our findings that elevated GLI expression is detected in 6 out of 11 aortic valves from patients with fibrotic aortic valves.

conclusionsOur data show that activating hedgehog signaling is sufficient to drive fibrosis in mice, and this mouse model is relevant to human aortic valve stenosis.

Indexed as

Aortic valveFibrosisHedgehogSmoothenedStenosis

Identifiers

PMID36864465
PMCPMC9983197
OpenAlexW4322767784

What OpenQuestion holds

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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.