Evidence map›Paper›PMID 28724751›Full record

ArticleCirculation2017

Tomo-Seq Identifies SOX9 as a Key Regulator of Cardiac Fibrosis During Ischemic Injury.

Grégory P A Lacraz, Jan Philipp Junker, Monika M Gladka, Bas Molenaar, Koen T Scholman, Marta Vigil-Garcia, Danielle Versteeg, Hesther de Ruiter, Marit W Vermunt, Menno P Creyghton and 4 more

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In one paragraph

Article in Circulation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
74citing papers in PubMed, 1 pooled it
6.6field-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

74 citing papers in PubMed, 1 synthesis or guideline pooled it, 118 citations in OpenAlex.

  1. Differential expression of members of SOX family of transcription factors in failing human hearts.Translational research : the journal of laboratory and clinical medicine · 2022
    Pooled it
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  19. Harnessing the regenerative potential ofbioRxiv : the preprint server for biology · 2024
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14 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

14 authors at 1 institution in 1 country.

Grégory P A LacrazFrom Hubrecht Institute, KNAW (G.P.A.L., J.P.J., M.M.G., B.M., K.T.S., M.V.-G., D.V., H.d.R., M.W.V., M.P.C., A.v.O., E.v.R.), Department of Pathology (M.M.H.H.), Department of Cardiology (N.d.J., E.v.R.), University Medical Center Utrecht, The Netherlands; and Berlin Institute for Medical Systems Biology, Max Delbrück Center for Molecular Medicine, Berlin, Germany (J.P.J.).
Jan Philipp JunkerFrom Hubrecht Institute, KNAW (G.P.A.L., J.P.J., M.M.G., B.M., K.T.S., M.V.-G., D.V., H.d.R., M.W.V., M.P.C., A.v.O., E.v.R.), Department of Pathology (M.M.H.H.), Department of Cardiology (N.d.J., E.v.R.), University Medical Center Utrecht, The Netherlands; and Berlin Institute for Medical Systems Biology, Max Delbrück Center for Molecular Medicine, Berlin, Germany (J.P.J.).
Monika M GladkaFrom Hubrecht Institute, KNAW (G.P.A.L., J.P.J., M.M.G., B.M., K.T.S., M.V.-G., D.V., H.d.R., M.W.V., M.P.C., A.v.O., E.v.R.), Department of Pathology (M.M.H.H.), Department of Cardiology (N.d.J., E.v.R.), University Medical Center Utrecht, The Netherlands; and Berlin Institute for Medical Systems Biology, Max Delbrück Center for Molecular Medicine, Berlin, Germany (J.P.J.).
Bas MolenaarFrom Hubrecht Institute, KNAW (G.P.A.L., J.P.J., M.M.G., B.M., K.T.S., M.V.-G., D.V., H.d.R., M.W.V., M.P.C., A.v.O., E.v.R.), Department of Pathology (M.M.H.H.), Department of Cardiology (N.d.J., E.v.R.), University Medical Center Utrecht, The Netherlands; and Berlin Institute for Medical Systems Biology, Max Delbrück Center for Molecular Medicine, Berlin, Germany (J.P.J.).
Koen T ScholmanFrom Hubrecht Institute, KNAW (G.P.A.L., J.P.J., M.M.G., B.M., K.T.S., M.V.-G., D.V., H.d.R., M.W.V., M.P.C., A.v.O., E.v.R.), Department of Pathology (M.M.H.H.), Department of Cardiology (N.d.J., E.v.R.), University Medical Center Utrecht, The Netherlands; and Berlin Institute for Medical Systems Biology, Max Delbrück Center for Molecular Medicine, Berlin, Germany (J.P.J.).
Marta Vigil-GarciaFrom Hubrecht Institute, KNAW (G.P.A.L., J.P.J., M.M.G., B.M., K.T.S., M.V.-G., D.V., H.d.R., M.W.V., M.P.C., A.v.O., E.v.R.), Department of Pathology (M.M.H.H.), Department of Cardiology (N.d.J., E.v.R.), University Medical Center Utrecht, The Netherlands; and Berlin Institute for Medical Systems Biology, Max Delbrück Center for Molecular Medicine, Berlin, Germany (J.P.J.).
Danielle VersteegFrom Hubrecht Institute, KNAW (G.P.A.L., J.P.J., M.M.G., B.M., K.T.S., M.V.-G., D.V., H.d.R., M.W.V., M.P.C., A.v.O., E.v.R.), Department of Pathology (M.M.H.H.), Department of Cardiology (N.d.J., E.v.R.), University Medical Center Utrecht, The Netherlands; and Berlin Institute for Medical Systems Biology, Max Delbrück Center for Molecular Medicine, Berlin, Germany (J.P.J.).
Hesther de RuiterFrom Hubrecht Institute, KNAW (G.P.A.L., J.P.J., M.M.G., B.M., K.T.S., M.V.-G., D.V., H.d.R., M.W.V., M.P.C., A.v.O., E.v.R.), Department of Pathology (M.M.H.H.), Department of Cardiology (N.d.J., E.v.R.), University Medical Center Utrecht, The Netherlands; and Berlin Institute for Medical Systems Biology, Max Delbrück Center for Molecular Medicine, Berlin, Germany (J.P.J.).
Marit W VermuntFrom Hubrecht Institute, KNAW (G.P.A.L., J.P.J., M.M.G., B.M., K.T.S., M.V.-G., D.V., H.d.R., M.W.V., M.P.C., A.v.O., E.v.R.), Department of Pathology (M.M.H.H.), Department of Cardiology (N.d.J., E.v.R.), University Medical Center Utrecht, The Netherlands; and Berlin Institute for Medical Systems Biology, Max Delbrück Center for Molecular Medicine, Berlin, Germany (J.P.J.).
Menno P CreyghtonFrom Hubrecht Institute, KNAW (G.P.A.L., J.P.J., M.M.G., B.M., K.T.S., M.V.-G., D.V., H.d.R., M.W.V., M.P.C., A.v.O., E.v.R.), Department of Pathology (M.M.H.H.), Department of Cardiology (N.d.J., E.v.R.), University Medical Center Utrecht, The Netherlands; and Berlin Institute for Medical Systems Biology, Max Delbrück Center for Molecular Medicine, Berlin, Germany (J.P.J.).
Manon M H HuibersFrom Hubrecht Institute, KNAW (G.P.A.L., J.P.J., M.M.G., B.M., K.T.S., M.V.-G., D.V., H.d.R., M.W.V., M.P.C., A.v.O., E.v.R.), Department of Pathology (M.M.H.H.), Department of Cardiology (N.d.J., E.v.R.), University Medical Center Utrecht, The Netherlands; and Berlin Institute for Medical Systems Biology, Max Delbrück Center for Molecular Medicine, Berlin, Germany (J.P.J.).
Nicolaas de JongeFrom Hubrecht Institute, KNAW (G.P.A.L., J.P.J., M.M.G., B.M., K.T.S., M.V.-G., D.V., H.d.R., M.W.V., M.P.C., A.v.O., E.v.R.), Department of Pathology (M.M.H.H.), Department of Cardiology (N.d.J., E.v.R.), University Medical Center Utrecht, The Netherlands; and Berlin Institute for Medical Systems Biology, Max Delbrück Center for Molecular Medicine, Berlin, Germany (J.P.J.).
Alexander van OudenaardenFrom Hubrecht Institute, KNAW (G.P.A.L., J.P.J., M.M.G., B.M., K.T.S., M.V.-G., D.V., H.d.R., M.W.V., M.P.C., A.v.O., E.v.R.), Department of Pathology (M.M.H.H.), Department of Cardiology (N.d.J., E.v.R.), University Medical Center Utrecht, The Netherlands; and Berlin Institute for Medical Systems Biology, Max Delbrück Center for Molecular Medicine, Berlin, Germany (J.P.J.).
Eva van RooijFrom Hubrecht Institute, KNAW (G.P.A.L., J.P.J., M.M.G., B.M., K.T.S., M.V.-G., D.V., H.d.R., M.W.V., M.P.C., A.v.O., E.v.R.), Department of Pathology (M.M.H.H.), Department of Cardiology (N.d.J., E.v.R.), University Medical Center Utrecht, The Netherlands; and Berlin Institute for Medical Systems Biology, Max Delbrück Center for Molecular Medicine, Berlin, Germany (J.P.J.). e.vanrooij@hubrecht.eu.
Amsterdam UMC Location Vrije Universiteit Amsterdam · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCardiac ischemic injury induces a pathological remodeling response, which can ultimately lead to heart failure. Detailed mechanistic insights into molecular signaling pathways relevant for different aspects of cardiac remodeling will support the identification of novel therapeutic targets.

methodsAlthough genome-wide transcriptome analysis on diseased tissues has greatly advanced our understanding of the regulatory networks that drive pathological changes in the heart, this approach has been disadvantaged by the fact that the signals are derived from tissue homogenates. Here we used tomo-seq to obtain a genome-wide gene expression signature with high spatial resolution spanning from the infarcted area to the remote to identify new regulators of cardiac remodeling. Cardiac tissue samples from patients suffering from ischemic heart disease were used to validate our findings.

resultsTracing transcriptional differences with a high spatial resolution across the infarcted heart enabled us to identify gene clusters that share a comparable expression profile. The spatial distribution patterns indicated a separation of expressional changes for genes involved in specific aspects of cardiac remodeling, such as fibrosis, cardiomyocyte hypertrophy, and calcium handling (

conclusionsBased on the exact local expression cues, tomo-seq can serve to reveal novel genes and key transcription factors involved in specific aspects of cardiac remodeling. Using tomo-seq, we were able to unveil the unknown relevance of SOX9 as a key regulator of cardiac fibrosis, pointing to SOX9 as a potential therapeutic target for cardiac fibrosis.

Indexed as

Gene Expression RegulationCollagen Type IFemaleFibrosisHigh-Throughput Nucleotide SequencingHumansMaleMuscle ProteinsMyocardial IschemiaMyocardiumSOX9 Transcription FactorCOL1A2 protein, humanCollagen Type IMuscle ProteinsSOX9 protein, humanSOX9 Transcription Factorfibrosismyocardial ischemiaSOX9 transcriptionventricular remodeling

Identifiers

PMID28724751
OpenAlexW2737798424

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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.