Evidence map›Paper›PMID 32441123›Full record

ArticleCirculation2020

Environment-Sensing Aryl Hydrocarbon Receptor Inhibits the Chondrogenic Fate of Modulated Smooth Muscle Cells in Atherosclerotic Lesions.

Juyong Brian Kim, Quanyi Zhao, Trieu Nguyen, Milos Pjanic, Paul Cheng, Robert Wirka, Stanislao Travisano, Manabu Nagao, Ramendra Kundu, Thomas Quertermous

Open access · bronzeAbstract read
In one paragraph

Article in Circulation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
68citing papers in PubMed, 3 pooled it
7.0field-weighted citation impact, top 2% 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

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

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Atherosclerotic Cell Fates: A Single-Cell View of ER Stress.Journal of cardiovascular development and disease · 2026
    Review
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8 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

10 authors at 1 institution in 1 country.

Juyong Brian KimDivision of Cardiovascular Medicine (J.B.K., Q.Z., T.N., M.P., P.C., R.W., S.T., M.N., R.K., T.Q.), Stanford University School of Medicine, CA.
Quanyi ZhaoDivision of Cardiovascular Medicine (J.B.K., Q.Z., T.N., M.P., P.C., R.W., S.T., M.N., R.K., T.Q.), Stanford University School of Medicine, CA.
Trieu NguyenDivision of Cardiovascular Medicine (J.B.K., Q.Z., T.N., M.P., P.C., R.W., S.T., M.N., R.K., T.Q.), Stanford University School of Medicine, CA.
Milos PjanicDivision of Cardiovascular Medicine (J.B.K., Q.Z., T.N., M.P., P.C., R.W., S.T., M.N., R.K., T.Q.), Stanford University School of Medicine, CA.
Paul ChengDivision of Cardiovascular Medicine (J.B.K., Q.Z., T.N., M.P., P.C., R.W., S.T., M.N., R.K., T.Q.), Stanford University School of Medicine, CA.
Robert WirkaDivision of Cardiovascular Medicine (J.B.K., Q.Z., T.N., M.P., P.C., R.W., S.T., M.N., R.K., T.Q.), Stanford University School of Medicine, CA.
Stanislao TravisanoDivision of Cardiovascular Medicine (J.B.K., Q.Z., T.N., M.P., P.C., R.W., S.T., M.N., R.K., T.Q.), Stanford University School of Medicine, CA.
Manabu NagaoDivision of Cardiovascular Medicine (J.B.K., Q.Z., T.N., M.P., P.C., R.W., S.T., M.N., R.K., T.Q.), Stanford University School of Medicine, CA.
Ramendra KunduDivision of Cardiovascular Medicine (J.B.K., Q.Z., T.N., M.P., P.C., R.W., S.T., M.N., R.K., T.Q.), Stanford University School of Medicine, CA.
Thomas QuertermousDivision of Cardiovascular Medicine (J.B.K., Q.Z., T.N., M.P., P.C., R.W., S.T., M.N., R.K., T.Q.), Stanford University School of Medicine, CA.
Cardiovascular Institute of the South · US

Funding

Stanford Islet Research CoreP30DK116074 · NIDDK · STANFORD UNIVERSITY · PI Seung K Kim · 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
Molecular Mechanisms of Insulin Resistance Associated LociR01DK107437 · NIDDK · STANFORD UNIVERSITY · PI QUERTERMOUS, THOMAS · 2016 to 2019
$2.2M
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
Capacity Building Assistance to Strengthen Public Health Immunization Infrastructure and PerformanceH23IP000999 · IP · ARIZONA STATE DEPARTMENT OF HLTH SRVCS · PI BHATTI, ALEXANDRA · 2015 to 2015
$818k
High Throughput DNA Sequencer UpgradeS10OD018220 · OD · STANFORD UNIVERSITY · PI COLLER, JOHN · 2014 to 2014
$596k
Four Laser, 18 Color Cell Sorter in the SSFFS10RR025518 · NCRR · STANFORD UNIVERSITY · PI HERZENBERG, LEONARD A · 2009 to 2009
$500k
The molecular mechanisms of SMAD3-mediated coronary disease riskF32HL143847 · NHLBI · STANFORD UNIVERSITY · PI CHENG, PAUL PO SHENG · 2018 to 2019
$114k
NCIRD CDC HHS H23 IP000999NCRR NIH HHS S10 RR025518NHLBI NIH HHS F32 HL143847NHLBI NIH HHS K08 HL133375NHLBI NIH HHS R01 HL109512NHLBI NIH HHS R01 HL134817NHLBI NIH HHS R01 HL139478NHLBI NIH HHS R01 HL145708NHLBI NIH HHS R33 HL120757NIDDK NIH HHS P30 DK116074NIDDK NIH HHS R01 DK107437NIH HHS S10 OD018220
6 · The paper itself

Abstract

backgroundSmooth muscle cells (SMC) play a critical role in atherosclerosis. The Aryl hydrocarbon receptor (AHR) is an environment-sensing transcription factor that contributes to vascular development, and has been implicated in coronary artery disease risk. We hypothesized that AHR can affect atherosclerosis by regulating phenotypic modulation of SMC.

methodsWe combined RNA-sequencing, chromatin immunoprecipitation followed by sequencing, assay for transposase-accessible chromatin using sequencing, and in vitro assays in human coronary artery SMCs, with single-cell RNA-sequencing, histology, and RNAscope in an SMC-specific lineage-tracing

resultsGenomic studies coupled with functional assays in cultured human coronary artery SMCs revealed that

conclusionsOverall, we conclude that

Indexed as

Alkaline PhosphataseAnimalsCell DifferentiationCell ProliferationCells, CulturedChondrogenesisCollagen Type IICoronary VesselsEnvironmental ExposureHumansMice, Inbred C57BLMice, KnockoutMyocytes, Smooth MusclePlaque, AtheroscleroticReceptors, Aryl HydrocarbonAlkaline PhosphataseALPL protein, humanCOL2A1 protein, humanCollagen Type IIReceptors, Aryl Hydrocarbonatherosclerosiscell differentiationmodels, animalmodels, geneticmuscle, smooth, vascularvascular calcification

Identifiers

PMID32441123
PMCPMC8066499
OpenAlexW3027019670

What OpenQuestion holds

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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.