Evidence map›Paper›PMID 28154134›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2017

Cdon deficiency causes cardiac remodeling through hyperactivation of WNT/β-catenin signaling.

Myong-Ho Jeong, Hyun-Ji Kim, Jung-Hoon Pyun, Kyu-Sil Choi, Dong I Lee, Soroosh Solhjoo, Brian O'Rourke, Gordon F Tomaselli, Dong Seop Jeong, Hana Cho and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
4.1field-weighted citation impact, top 5% 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

41 citing papers in PubMed, 64 citations in OpenAlex.

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  18. The role of β-catenin in cardiac diseases.Frontiers in pharmacology · 2023
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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

11 authors at 6 institutions in 2 countries.

Myong-Ho JeongDepartment of Molecular Cell Biology, Sungkyunkwan University School of Medicine, Suwon, Korea 16419.
Hyun-Ji KimSamsung Biomedical Research Institute, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea 06351.
Jung-Hoon PyunDepartment of Molecular Cell Biology, Sungkyunkwan University School of Medicine, Suwon, Korea 16419.
Kyu-Sil ChoiSamsung Biomedical Research Institute, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea 06351.
Dong I LeeDivision of Cardiology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205.
Soroosh SolhjooDivision of Cardiology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205.
Brian O'RourkeDivision of Cardiology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205.
Gordon F TomaselliDivision of Cardiology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205.
Dong Seop JeongDepartment of Thoracic and Cardiovascular Surgery, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea 06351.
Hana ChoSamsung Biomedical Research Institute, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea 06351; kangj01@skku.edu hanacho@skku.edu.
Jong-Sun KangDepartment of Molecular Cell Biology, Sungkyunkwan University School of Medicine, Suwon, Korea 16419; kangj01@skku.edu hanacho@skku.edu.
Biomedical Research Institute · USJohns Hopkins Medicine · USJohns Hopkins University · USSamsung Medical Center · KRSungkyunkwan University · KRSamsung (United States) · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

On pathological stress, Wnt signaling is reactivated and induces genes associated with cardiac remodeling and fibrosis. We have previously shown that a cell surface receptor Cdon (cell-adhesion associated, oncogene regulated) suppresses Wnt signaling to promote neuronal differentiation however its role in heart is unknown. Here, we demonstrate a critical role of Cdon in cardiac function and remodeling. Cdon is expressed and predominantly localized at intercalated disk in both mouse and human hearts. Cdon-deficient mice develop cardiac dysfunction including reduced ejection fraction and ECG abnormalities.

Indexed as

Animalsbeta CateninCell Adhesion MoleculesConnexin 43ConnexinsFibrosisGap JunctionsHeartMiceMice, Inbred C57BLMyocardiumMyocytes, CardiacPyrimidinesPyrrolesRatsRats, Sprague-Dawleybeta CateninCdon protein, mouseCell Adhesion MoleculesConnexin 43ConnexinsPyrimidinesPyrrolesTWS 119cardiac fibrosisCdonconnexin 43gap junctionWnt

Identifiers

PMID28154134
PMCPMC5338397
OpenAlexW2586007853

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.