Evidence map›Paper›PMID 36852690›Full record

ArticleCirculation research2023

Discovery of Transacting Long Noncoding RNAs That Regulate Smooth Muscle Cell Phenotype.

Huitong Shi, Trieu Nguyen, Quanyi Zhao, Paul Cheng, Disha Sharma, Hyun-Jung Kim, Juyong Brian Kim, Robert Wirka, Chad S Weldy, João P Monteiro and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Circulation research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

7 citing papers in PubMed, 9 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Long Non-Coding RNA Function in Smooth Muscle Cell Plasticity and Atherosclerosis.Arteriosclerosis, thrombosis, and vascular biology · 2025
    Review
  5. Article
  6. Review
  7. 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 2 institutions in 1 country.

Huitong Shi *Division of Cardiovascular Medicine and Cardiovascular Institute, School of Medicine, Stanford University (H.S., T.N., Q.Z., P.C., D.S., H.-J.K., J.B.K., C.S.W., J.P.M., T.Q.).
Trieu Nguyen *Division of Cardiovascular Medicine and Cardiovascular Institute, School of Medicine, Stanford University (H.S., T.N., Q.Z., P.C., D.S., H.-J.K., J.B.K., C.S.W., J.P.M., T.Q.).ORCID 0000-0001-5647-1301
Quanyi ZhaoDivision of Cardiovascular Medicine and Cardiovascular Institute, School of Medicine, Stanford University (H.S., T.N., Q.Z., P.C., D.S., H.-J.K., J.B.K., C.S.W., J.P.M., T.Q.).
Paul ChengDivision of Cardiovascular Medicine and Cardiovascular Institute, School of Medicine, Stanford University (H.S., T.N., Q.Z., P.C., D.S., H.-J.K., J.B.K., C.S.W., J.P.M., T.Q.).
Disha SharmaDivision of Cardiovascular Medicine and Cardiovascular Institute, School of Medicine, Stanford University (H.S., T.N., Q.Z., P.C., D.S., H.-J.K., J.B.K., C.S.W., J.P.M., T.Q.).ORCID 0000-0001-9486-2709
Hyun-Jung KimDivision of Cardiovascular Medicine and Cardiovascular Institute, School of Medicine, Stanford University (H.S., T.N., Q.Z., P.C., D.S., H.-J.K., J.B.K., C.S.W., J.P.M., T.Q.).ORCID 0000-0001-6264-0220
Juyong Brian KimDivision of Cardiovascular Medicine and Cardiovascular Institute, School of Medicine, Stanford University (H.S., T.N., Q.Z., P.C., D.S., H.-J.K., J.B.K., C.S.W., J.P.M., T.Q.).ORCID 0000-0002-9675-2607
Robert WirkaDepartments of Medicine and Cell Biology and Physiology, and McAllister Heart Institute, University of North Carolina at Chapel Hill (R.W.).ORCID 0000-0001-9131-9508
Chad S WeldyDivision of Cardiovascular Medicine and Cardiovascular Institute, School of Medicine, Stanford University (H.S., T.N., Q.Z., P.C., D.S., H.-J.K., J.B.K., C.S.W., J.P.M., T.Q.).ORCID 0000-0003-4652-6422
João P MonteiroDivision of Cardiovascular Medicine and Cardiovascular Institute, School of Medicine, Stanford University (H.S., T.N., Q.Z., P.C., D.S., H.-J.K., J.B.K., C.S.W., J.P.M., T.Q.).
Thomas QuertermousDivision of Cardiovascular Medicine and Cardiovascular Institute, School of Medicine, Stanford University (H.S., T.N., Q.Z., P.C., D.S., H.-J.K., J.B.K., C.S.W., J.P.M., T.Q.).ORCID 0000-0002-7645-9067
Cardiovascular Institute of the South · USUniversity of North Carolina at Chapel Hill · US

Funding

Stanford Center for Connecting DNA Variants to Function and PhenotypeUM1HG011972 · NHGRI · STANFORD UNIVERSITY · PI JESSE M ENGREITZ, THOMAS QUERTERMOUS · 2021 to 2026
$10.5M
Causal variant association mechanisms in TCF21 binding coronary disease lociR01HL134817 · NHLBI · STANFORD UNIVERSITY · PI THOMAS QUERTERMOUS · 2017 to 2026
$6.2M
The SMAD3 signaling network in coronary artery disease riskR01HL139478 · NHLBI · STANFORD UNIVERSITY · PI THOMAS QUERTERMOUS · 2018 to 2026
$3.7M
PDGFD regulates a transcriptional network to modulate smooth muscle cell transition and coronary artery disease riskR01HL156846 · NHLBI · STANFORD UNIVERSITY · PI QUERTERMOUS, THOMAS · 2021 to 2024
$2.7M
Identifying tobacco-genetic interactions through study of the aryl hydrocarbon receptor pathway.R01HL151535 · NHLBI · STANFORD UNIVERSITY · PI QUERTERMOUS, THOMAS · 2021 to 2024
$2.7M
LncRNA Transcriptional Mechanisms of Coronary Artery Disease RiskR01HL145708 · NHLBI · STANFORD UNIVERSITY · PI QUERTERMOUS, THOMAS · 2019 to 2022
$1.6M
From Locus to Function: Role of ZEB2 in Human Risk of Coronary Artery DiseaseK08HL153798 · NHLBI · STANFORD UNIVERSITY · PI CHENG, PAUL PO SHENG · 2020 to 2024
$933k
Regulation of Inflammation and Atherosclerosis by TCF21K08HL133375 · NHLBI · STANFORD UNIVERSITY · PI KIM, JUYONG BRIAN · 2016 to 2020
$840k
The role of TWIST1 in smooth muscle cells during atherosclerosisK08HL152308 · NHLBI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI WIRKA, ROBERT · 2020 to 2024
$765k
ADAR mediated RNA editing is a causal mechanism in coronary artery diseaseK08HL167699 · NHLBI · STANFORD UNIVERSITY · PI Chad S Weldy · 2023 to 2026
$664k
A transcriptional network which governs smooth muscle transition is mediated by causal coronary artery disease gene PDGFDF32HL160067 · NHLBI · STANFORD UNIVERSITY · PI WELDY, CHAD S · 2021 to 2022
$135k
NHGRI NIH HHS UM1 HG011972NHLBI NIH HHS F32 HL160067NHLBI NIH HHS K08 HL133375NHLBI NIH HHS K08 HL152308NHLBI NIH HHS K08 HL153798NHLBI NIH HHS K08 HL167699NHLBI NIH HHS L30 HL159413NHLBI NIH HHS R01 HL134817NHLBI NIH HHS R01 HL139478NHLBI NIH HHS R01 HL145708NHLBI NIH HHS R01 HL151535NHLBI NIH HHS R01 HL156846
6 · The paper itself

Abstract

backgroundSmooth muscle cells (SMC), the major cell type in atherosclerotic plaques, are vital in coronary artery diseases (CADs). SMC phenotypic transition, which leads to the formation of various cell types in atherosclerotic plaques, is regulated by a network of genetic and epigenetic mechanisms and governs the risk of disease. The involvement of long noncoding RNAs (lncRNAs) has been increasingly identified in cardiovascular disease. However, SMC lncRNAs have not been comprehensively characterized, and their regulatory role in SMC state transition remains unknown.

methodsA discovery pipeline was constructed and applied to deeply strand-specific RNA sequencing from perturbed human coronary artery SMC with different disease-related stimuli, to allow for the detection of novel lncRNAs. The functional relevance of a select few novel lncRNAs were verified in vitro.

resultsWe identified 4579 known and 13 655 de novo lncRNAs in human coronary artery SMC. Consistent with previous long noncoding RNA studies, these lncRNAs overall have fewer exons, are shorter in length than protein-coding genes (pcGenes), and have relatively low expression level. Genomic location of these long noncoding RNA is disproportionately enriched near CAD-related TFs (transcription factors), genetic loci, and gene regulators of SMC identity, suggesting the importance of their function in disease. Two de novo lncRNAs,

conclusionsExpression of a large and diverse set of lncRNAs in human coronary artery SMC are highly dynamic in response to CAD-related stimuli. The dynamic changes in expression of these lncRNAs correspond to alterations in transcriptional programs that are relevant to CAD, suggesting a critical role for lncRNAs in SMC phenotypic transition and human atherosclerotic disease.

Indexed as

Plaque, AtheroscleroticRNA, Long NoncodingHumansMyocytes, Smooth MusclePhenotypeTranscription FactorsRNA, Long NoncodingTranscription Factorscoronary artery diseaselong-noncoding RNAphenotypic transitionsmooth muscle cell

Identifiers

PMID36852690
PMCPMC11056793
OpenAlexW4322617276

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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.