Evidence map›Paper›PMID 31815603›Full record

ArticleCirculation research2020

Coronary Disease-Associated Gene

Manabu Nagao, Qing Lyu, Quanyi Zhao, Robert C Wirka, Joetsaroop Bagga, Trieu Nguyen, Paul Cheng, Juyong Brian Kim, Milos Pjanic, Joseph M Miano and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Circulation research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
75citing papers in PubMed, 2 pooled it
3.3field-weighted citation impact, top 7% 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

75 citing papers in PubMed, 2 syntheses or guidelines pooled it, 99 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
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  4. Article
  5. Article
  6. The transcription factor Tcf21 is necessary for adoption of cell fates byAmerican journal of physiology. Renal physiology · 2026
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15 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 2 institutions in 1 country.

Manabu NagaoFrom the Division of Cardiovascular Medicine, Cardiovascular Institute, Stanford University School of Medicine, CA (M.N., Q.Z., R.C.W., J.B., T.N., P.C., J.B.K., M.P., T.Q.).
Qing LyuAab Cardiovascular Research Institute, University of Rochester School of Medicine and Dentistry, NY (Q.L., J.M.M.).
Quanyi ZhaoFrom the Division of Cardiovascular Medicine, Cardiovascular Institute, Stanford University School of Medicine, CA (M.N., Q.Z., R.C.W., J.B., T.N., P.C., J.B.K., M.P., T.Q.).
Robert C WirkaFrom the Division of Cardiovascular Medicine, Cardiovascular Institute, Stanford University School of Medicine, CA (M.N., Q.Z., R.C.W., J.B., T.N., P.C., J.B.K., M.P., T.Q.).
Joetsaroop BaggaFrom the Division of Cardiovascular Medicine, Cardiovascular Institute, Stanford University School of Medicine, CA (M.N., Q.Z., R.C.W., J.B., T.N., P.C., J.B.K., M.P., T.Q.).
Trieu NguyenFrom the Division of Cardiovascular Medicine, Cardiovascular Institute, Stanford University School of Medicine, CA (M.N., Q.Z., R.C.W., J.B., T.N., P.C., J.B.K., M.P., T.Q.).
Paul ChengFrom the Division of Cardiovascular Medicine, Cardiovascular Institute, Stanford University School of Medicine, CA (M.N., Q.Z., R.C.W., J.B., T.N., P.C., J.B.K., M.P., T.Q.).
Juyong Brian KimFrom the Division of Cardiovascular Medicine, Cardiovascular Institute, Stanford University School of Medicine, CA (M.N., Q.Z., R.C.W., J.B., T.N., P.C., J.B.K., M.P., T.Q.).
Milos PjanicFrom the Division of Cardiovascular Medicine, Cardiovascular Institute, Stanford University School of Medicine, CA (M.N., Q.Z., R.C.W., J.B., T.N., P.C., J.B.K., M.P., T.Q.).
Joseph M MianoAab Cardiovascular Research Institute, University of Rochester School of Medicine and Dentistry, NY (Q.L., J.M.M.).
Thomas QuertermousFrom the Division of Cardiovascular Medicine, Cardiovascular Institute, Stanford University School of Medicine, CA (M.N., Q.Z., R.C.W., J.B., T.N., P.C., J.B.K., M.P., T.Q.).
Stanford University · USCardiovascular Institute of the South · US

Funding

Stanford Islet Research CoreP30DK116074 · NIDDK · STANFORD UNIVERSITY · PI FREDRIC B. KRAEMER · 2017 to 2026
$19.5M
Causal variant association mechanisms in TCF21 binding coronary disease lociR01HL134817 · NHLBI · STANFORD UNIVERSITY · PI THOMAS QUERTERMOUS · 2017 to 2026
$6.2M
Mechanism of the Coronary Heart Disease Association at Chromosome 6q23.2R01HL109512 · NHLBI · STANFORD UNIVERSITY · PI QUERTERMOUS, THOMAS · 2011 to 2019
$6.1M
The SMAD3 signaling network in coronary artery disease riskR01HL139478 · NHLBI · STANFORD UNIVERSITY · PI THOMAS QUERTERMOUS · 2018 to 2026
$3.7M
Transcriptional Control of Myocardin and the MYOCARDomeR01HL138987 · NHLBI · UNIVERSITY OF ROCHESTER · PI MIANO, JOSEPH M · 2018 to 2021
$2.3M
Molecular Mechanisms of Insulin Resistance Associated LociR01DK107437 · NIDDK · STANFORD UNIVERSITY · PI QUERTERMOUS, THOMAS · 2016 to 2019
$2.2M
Regulation and Function of SRF in Vascular PathiobiologyR01HL147476 · NHLBI · UNIVERSITY OF ROCHESTER · PI MIANO, JOSEPH M · 2019 to 2022
$2.1M
LncRNA Transcriptional Mechanisms of Coronary Artery Disease RiskR01HL145708 · NHLBI · STANFORD UNIVERSITY · PI QUERTERMOUS, THOMAS · 2019 to 2022
$1.6M
Identification of causal coronary heart disease variation in smooth muscle cellsR33HL120757 · NHLBI · STANFORD UNIVERSITY · PI QUERTERMOUS, THOMAS · 2016 to 2018
$1.6M
Regulation of Inflammation and Atherosclerosis by TCF21K08HL133375 · NHLBI · STANFORD UNIVERSITY · PI KIM, JUYONG BRIAN · 2016 to 2020
$840k
The molecular mechanisms of SMAD3-mediated coronary disease riskF32HL143847 · NHLBI · STANFORD UNIVERSITY · PI CHENG, PAUL PO SHENG · 2018 to 2019
$114k
NHLBI NIH HHS F32 HL143847NHLBI NIH HHS K08 HL133375NHLBI NIH HHS R01 HL109512NHLBI NIH HHS R01 HL134817NHLBI NIH HHS R01 HL138987NHLBI NIH HHS R01 HL139478NHLBI NIH HHS R01 HL145708NHLBI NIH HHS R01 HL147476NHLBI NIH HHS R33 HL120757NIDDK NIH HHS P30 DK116074NIDDK NIH HHS R01 DK107437
6 · The paper itself

Abstract

rationaleThe gene encoding TCF21 (transcription factor 21) has been linked to coronary artery disease risk by human genome-wide association studies in multiple racial ethnic groups. In murine models, Tcf21 is required for phenotypic modulation of smooth muscle cells (SMCs) in atherosclerotic tissues and promotes a fibroblast phenotype in these cells. In humans, TCF21 expression inhibits risk for coronary artery disease. The molecular mechanism by which TCF21 regulates SMC phenotype is not known.

objectiveTo better understand how TCF21 affects the SMC phenotype, we sought to investigate the possible mechanisms by which it regulates the lineage determining MYOCD (myocardin)-SRF (serum response factor) pathway. METHODS AND

resultsModulation of

conclusionsThese data indicate that

Indexed as

Base SequenceBasic Helix-Loop-Helix ProteinsBinding SitesCell DifferentiationCells, CulturedCoronary Artery DiseaseGene Expression RegulationGenetic Predisposition to DiseaseHEK293 CellsHumansMyocardinMyocytes, Smooth MuscleNuclear ProteinsPromoter Regions, GeneticProtein BindingSerum Response FactorBasic Helix-Loop-Helix ProteinsMyocardinNuclear ProteinsSerum Response FactorTCF21 protein, humanTrans-Activatorsatherosclerosiscoronary circulationgene expressiongeneticsgenomics

Identifiers

PMID31815603
PMCPMC7274203
OpenAlexW2991973734

What OpenQuestion holds

Textmetadata
LicenceTDM
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.