Evidence map›Paper›PMID 26896382›Full record

ArticleCirculation. Cardiovascular genetics2016

Systematic Characterization of Long Noncoding RNAs Reveals the Contrasting Coordination of Cis- and Trans-Molecular Regulation in Human Fetal and Adult Hearts.

Chunjiang He, Hanyang Hu, Kitchener D Wilson, Haodi Wu, Jing Feng, Siyu Xia, Jared Churko, Kun Qu, Howard Y Chang, Joseph C Wu

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

Article in Circulation. Cardiovascular genetics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 1 pooled it
3.5field-weighted citation impact, top 8% 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

29 citing papers in PubMed, 1 synthesis or guideline pooled it, 47 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Inhibition of Long Noncoding RNAMolecular and cellular biology · 2021
    Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Long Non-coding RNA ECRAR Triggers Post-natal Myocardial Regeneration by Activating ERK1/2 Signaling.Molecular therapy : the journal of the American Society of Gene Therapy · 2019
    Article
  14. Article
  15. LncRNA-Theranostics · 2019
    Article
  16. A Allele ofOpen life sciences · 2019
    Article
  17. Article
  18. Review
  19. Article
  20. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 1 institution in 2 countries.

Chunjiang HeFrom the Stanford Cardiovascular Institute (C.H., K.D.W., H.W., J.C., J.C.W.), Division of Cardiology, Department of Medicine (C.H., H.W., J.C., J.C.W.), Department of Pathology (K.D.W.), and Program in Epithelial Biology (K.Q., H.Y.C.), Stanford University, CA; and School of Basic Medical Science (C.H., H.H., S.X.) and International School of Software (J.F.), Wuhan University, Wuhan, China. joewu@stanford.edu che@whu.edu.cn.
Hanyang HuFrom the Stanford Cardiovascular Institute (C.H., K.D.W., H.W., J.C., J.C.W.), Division of Cardiology, Department of Medicine (C.H., H.W., J.C., J.C.W.), Department of Pathology (K.D.W.), and Program in Epithelial Biology (K.Q., H.Y.C.), Stanford University, CA; and School of Basic Medical Science (C.H., H.H., S.X.) and International School of Software (J.F.), Wuhan University, Wuhan, China.
Kitchener D WilsonFrom the Stanford Cardiovascular Institute (C.H., K.D.W., H.W., J.C., J.C.W.), Division of Cardiology, Department of Medicine (C.H., H.W., J.C., J.C.W.), Department of Pathology (K.D.W.), and Program in Epithelial Biology (K.Q., H.Y.C.), Stanford University, CA; and School of Basic Medical Science (C.H., H.H., S.X.) and International School of Software (J.F.), Wuhan University, Wuhan, China.
Haodi WuFrom the Stanford Cardiovascular Institute (C.H., K.D.W., H.W., J.C., J.C.W.), Division of Cardiology, Department of Medicine (C.H., H.W., J.C., J.C.W.), Department of Pathology (K.D.W.), and Program in Epithelial Biology (K.Q., H.Y.C.), Stanford University, CA; and School of Basic Medical Science (C.H., H.H., S.X.) and International School of Software (J.F.), Wuhan University, Wuhan, China.
Jing FengFrom the Stanford Cardiovascular Institute (C.H., K.D.W., H.W., J.C., J.C.W.), Division of Cardiology, Department of Medicine (C.H., H.W., J.C., J.C.W.), Department of Pathology (K.D.W.), and Program in Epithelial Biology (K.Q., H.Y.C.), Stanford University, CA; and School of Basic Medical Science (C.H., H.H., S.X.) and International School of Software (J.F.), Wuhan University, Wuhan, China.
Siyu XiaFrom the Stanford Cardiovascular Institute (C.H., K.D.W., H.W., J.C., J.C.W.), Division of Cardiology, Department of Medicine (C.H., H.W., J.C., J.C.W.), Department of Pathology (K.D.W.), and Program in Epithelial Biology (K.Q., H.Y.C.), Stanford University, CA; and School of Basic Medical Science (C.H., H.H., S.X.) and International School of Software (J.F.), Wuhan University, Wuhan, China.
Jared ChurkoFrom the Stanford Cardiovascular Institute (C.H., K.D.W., H.W., J.C., J.C.W.), Division of Cardiology, Department of Medicine (C.H., H.W., J.C., J.C.W.), Department of Pathology (K.D.W.), and Program in Epithelial Biology (K.Q., H.Y.C.), Stanford University, CA; and School of Basic Medical Science (C.H., H.H., S.X.) and International School of Software (J.F.), Wuhan University, Wuhan, China.
Kun QuFrom the Stanford Cardiovascular Institute (C.H., K.D.W., H.W., J.C., J.C.W.), Division of Cardiology, Department of Medicine (C.H., H.W., J.C., J.C.W.), Department of Pathology (K.D.W.), and Program in Epithelial Biology (K.Q., H.Y.C.), Stanford University, CA; and School of Basic Medical Science (C.H., H.H., S.X.) and International School of Software (J.F.), Wuhan University, Wuhan, China.
Howard Y ChangFrom the Stanford Cardiovascular Institute (C.H., K.D.W., H.W., J.C., J.C.W.), Division of Cardiology, Department of Medicine (C.H., H.W., J.C., J.C.W.), Department of Pathology (K.D.W.), and Program in Epithelial Biology (K.Q., H.Y.C.), Stanford University, CA; and School of Basic Medical Science (C.H., H.H., S.X.) and International School of Software (J.F.), Wuhan University, Wuhan, China.
Joseph C WuFrom the Stanford Cardiovascular Institute (C.H., K.D.W., H.W., J.C., J.C.W.), Division of Cardiology, Department of Medicine (C.H., H.W., J.C., J.C.W.), Department of Pathology (K.D.W.), and Program in Epithelial Biology (K.Q., H.Y.C.), Stanford University, CA; and School of Basic Medical Science (C.H., H.H., S.X.) and International School of Software (J.F.), Wuhan University, Wuhan, China. joewu@stanford.edu che@whu.edu.cn.
Wuhan University · CN

Funding

Project 3: Effect of Age and Longevity Genes on Epigenomic MechanismsP01GM099130 · NIGMS · STANFORD UNIVERSITY · PI SNYDER, MICHAEL P. · 2011 to 2015
$11.4M
Elucidating Mechanism of Cardiac Fibrosis with Cell Village of Pooled Human iPSCsR01HL130020 · NHLBI · STANFORD UNIVERSITY · PI Ronglih Liao, MARK MERCOLA · 2016 to 2026
$7.3M
Genome Editing of Human iPSCs to Study Inherited Hypertrophic CardiomyopathyR01HL126527 · NHLBI · STANFORD UNIVERSITY · PI QI, LEI STANLEY, WU, JOSEPH C. · 2015 to 2022
$5.4M
Modeling Susceptibility to Chemotherapy-Induced Cardiotoxicity Using Human iPSCsR01HL123968 · NHLBI · STANFORD UNIVERSITY · PI QUERTERMOUS, THOMAS, WU, JOSEPH C. · 2014 to 2021
$4.8M
A Systems Biology Approach to Study Cardiac Arrhythmias: iPS Cells and In Silico ModelingR01HL128170 · NHLBI · STANFORD UNIVERSITY · PI ALTMAN, RUSS BIAGIO, CLANCY, COLLEEN E · 2015 to 2018
$3.0M
NHLBI NIH HHS R01 HL123968NHLBI NIH HHS R01 HL126527NHLBI NIH HHS R01 HL128170NHLBI NIH HHS R01 HL130020NHLBI NIH HHS R01HL130020NIGMS NIH HHS P01 GM099130
6 · The paper itself

Abstract

backgroundThe molecular regulation of heart development is regulated by cis- and trans-factors acting on the genome and epigenome. As a class of important regulatory RNAs, the role of long noncoding RNAs (lncRNAs) in human heart development is still poorly understood. Furthermore, factors that interact with lncRNAs in this process are not well characterized. METHODS AND

resultsUsing RNA sequencing, we systematically define the contrasting lncRNA expression patterns between fetal and adult hearts. We report that lncRNAs upregulated in adult versus fetal heart have different sequence features and distributions. For example, the adult heart expresses more sense lncRNAs compared with fetal heart. We also report the coexpression of lncRNAs and neighboring coding genes that have important functions in heart development. Importantly, the regulation of lncRNA expression during fetal to adult heart development seems to be due, in part, to the coordination of specific developmental epigenetic modifications, such as H3K4me1 and H3k4me3. The expression of promoter-associated lncRNAs in adult and fetal hearts also seems to be related to these epigenetic states. Finally, transcription factor-binding analysis suggests that lncRNAs are directly regulating cardiac gene expression during development.

conclusionsWe provide a systematic analysis of lncRNA control of heart development that gives clues to the roles that specific lncRNAs play in fetal and adult hearts.

Indexed as

Gene Expression Regulation, DevelopmentalAdultEpigenesis, GeneticFetusGene Regulatory NetworksHeartHumansOpen Reading FramesPolymorphism, Single NucleotideProtein BindingRNA, Long NoncodingTranscription FactorsRNA, Long NoncodingTranscription Factorsfetal heartgene expressiongenomicslong noncoding RNAstranscription factor

Identifiers

PMID26896382
PMCPMC4862831
OpenAlexW2280074825

What OpenQuestion holds

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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.