Evidence map›Paper›PMID 28621328›Full record

ArticleCell research2017

Live cell screening platform identifies PPARδ as a regulator of cardiomyocyte proliferation and cardiac repair.

Ajit Magadum, Yishu Ding, Lan He, Teayoun Kim, Mohankrishna Dalvoy Vasudevarao, Qinqiang Long, Kevin Yang, Nadeera Wickramasinghe, Harsha V Renikunta, Nicole Dubois and 3 more

Open access · hybridAbstract read
In one paragraph

Article in Cell research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed, 1 pooled it
3.6field-weighted citation impact, top 6% 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

65 citing papers in PubMed, 1 synthesis or guideline pooled it, 82 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Signaling pathways regulating cardiac regeneration.Cell regeneration (London, England) · 2026
    Review
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  14. Nuclear Receptor ERRγ Protects Against Cardiac Ischemic Injury by Suppressing GBP5-Mediated Myocardial Inflammation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
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5 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

13 authors at 5 institutions in 3 countries.

Ajit MagadumDepartment of Cardiac Development and Remodelling, Max-Planck-Institute for Heart and Lung Research, Parkstrasse 1, Bad Nauheim 61231, Germany.
Yishu DingDepartment of Nutrition Sciences, University of Alabama at Birmingham, 1675 University Blvd, Birmingham, AL 35294-3360, USA.
Lan HeDepartment of Nutrition Sciences, University of Alabama at Birmingham, 1675 University Blvd, Birmingham, AL 35294-3360, USA.
Teayoun KimDepartment of Nutrition Sciences, University of Alabama at Birmingham, 1675 University Blvd, Birmingham, AL 35294-3360, USA.
Mohankrishna Dalvoy VasudevaraoInstitute of Biochemistry and Molecular Biology, Ulm University, Albert-Einstein-Allee 11, Ulm 89081, Germany.
Qinqiang LongDepartment of Nutrition Sciences, University of Alabama at Birmingham, 1675 University Blvd, Birmingham, AL 35294-3360, USA.
Kevin YangDepartment of Nutrition Sciences, University of Alabama at Birmingham, 1675 University Blvd, Birmingham, AL 35294-3360, USA.
Nadeera WickramasingheDepartment for Cell, Developmental and Regenerative Biology, Icahn School of Medicine at Mount Sinai, 1470 Madison Avenue, Box 1040, New York, NY 10029, USA.
Harsha V RenikuntaDepartment of Cardiac Development and Remodelling, Max-Planck-Institute for Heart and Lung Research, Parkstrasse 1, Bad Nauheim 61231, Germany.
Nicole DuboisDepartment for Cell, Developmental and Regenerative Biology, Icahn School of Medicine at Mount Sinai, 1470 Madison Avenue, Box 1040, New York, NY 10029, USA.
Gilbert WeidingerInstitute of Biochemistry and Molecular Biology, Ulm University, Albert-Einstein-Allee 11, Ulm 89081, Germany.
Qinglin YangDepartment of Nutrition Sciences, University of Alabama at Birmingham, 1675 University Blvd, Birmingham, AL 35294-3360, USA.
Felix B EngelDepartment of Cardiac Development and Remodelling, Max-Planck-Institute for Heart and Lung Research, Parkstrasse 1, Bad Nauheim 61231, Germany.
University of Alabama at Birmingham · USIcahn School of Medicine at Mount Sinai · USMax Planck Institute for Heart and Lung Research · DEUniversität Ulm · DEFriedrich-Alexander-Universität Erlangen-Nürnberg · DE

Funding

University of Alabama at Birmingham's Diabetes Research CenterP30DK079626 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI Kirk Michael Habegger · 2013 to 2026
$19.5M
Improving Mitochondrial Function to Protect against Myocardial Ischemia/ReperfusionR01HL135336 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI YANG, QINGLIN · 2017 to 2020
$1.5M
Restore Energy Capacity in the Aging HeartR03AG055899 · NIA · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI YANG, QINGLIN · 2017 to 2018
$149k
NHLBI NIH HHS R01 HL135336NIA NIH HHS R03 AG055899NIDDK NIH HHS P30 DK079626
6 · The paper itself

Abstract

Zebrafish can efficiently regenerate their heart through cardiomyocyte proliferation. In contrast, mammalian cardiomyocytes stop proliferating shortly after birth, limiting the regenerative capacity of the postnatal mammalian heart. Therefore, if the endogenous potential of postnatal cardiomyocyte proliferation could be enhanced, it could offer a promising future therapy for heart failure patients. Here, we set out to systematically identify small molecules triggering postnatal cardiomyocyte proliferation. By screening chemical compound libraries utilizing a Fucci-based system for assessing cell cycle stages, we identified carbacyclin as an inducer of postnatal cardiomyocyte proliferation. In vitro, carbacyclin induced proliferation of neonatal and adult mononuclear rat cardiomyocytes via a peroxisome proliferator-activated receptor δ (PPARδ)/PDK1/p308Akt/GSK3β/β-catenin pathway. Inhibition of PPARδ reduced cardiomyocyte proliferation during zebrafish heart regeneration. Notably, inducible cardiomyocyte-specific overexpression of constitutively active PPARδ as well as treatment with PPARδ agonist after myocardial infarction in mice induced cell cycle progression in cardiomyocytes, reduced scarring, and improved cardiac function. Collectively, we established a cardiomyocyte proliferation screening system and present a new drugable target with promise for the treatment of cardiac pathologies caused by cardiomyocyte loss.

Indexed as

AnimalsCardiomyopathiesCell ProliferationEpoprostenolMyocardiumMyocytes, CardiacPPAR deltaRatsRats, Sprague-DawleySignal TransductionZebrafishZebrafish ProteinscarboprostacyclinEpoprostenolPPAR deltaZebrafish Proteins

Identifiers

PMID28621328
PMCPMC5539351
OpenAlexW2625547916

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.