Evidence map›Paper›PMID 28871043›Full record

ArticleJournal of the American Heart Association2017

MMI-0100 Inhibits Cardiac Fibrosis in a Mouse Model Overexpressing Cardiac Myosin Binding Protein C.

Qinghang Meng, Bidur Bhandary, Hanna Osinska, Jeanne James, Na Xu, Kritton Shay-Winkler, James Gulick, Monte S Willis, Cynthia Lander, Jeffrey Robbins

Open access · goldAbstract read
In one paragraph

Article in Journal of the American Heart Association, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.2field-weighted citation impact, top 18% 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

14 citing papers in PubMed, 15 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. Review
  8. Mangiferin ameliorates cardiac fibrosis in D-galactose-induced aging rats by inhibiting TGF-β/p38/MK2 signaling pathway.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2021
    Article
  9. The Role of NLRP3 Inflammasome in Radiation-Induced Cardiovascular Injury.Frontiers in cell and developmental biology · 2020
    Review
  10. Cardiac Fibroblast p38 MAPK: A Critical Regulator of Myocardial Remodeling.Journal of cardiovascular development and disease · 2019
    Review
  11. Article
  12. Article
  13. Article
  14. 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

10 authors at 4 institutions in 1 country.

Qinghang MengDivision of Molecular Cardiovascular Biology, The Heart Institute Cincinnati Children's Hospital, Cincinnati, OH.
Bidur BhandaryDivision of Molecular Cardiovascular Biology, The Heart Institute Cincinnati Children's Hospital, Cincinnati, OH.
Hanna OsinskaDivision of Molecular Cardiovascular Biology, The Heart Institute Cincinnati Children's Hospital, Cincinnati, OH.
Jeanne JamesChildren's Hospital of Wisconsin-Milwaukee Campus, Milwaukee, WI.
Na XuDivision of Molecular Cardiovascular Biology, The Heart Institute Cincinnati Children's Hospital, Cincinnati, OH.
Kritton Shay-WinklerDivision of Molecular Cardiovascular Biology, The Heart Institute Cincinnati Children's Hospital, Cincinnati, OH.
James GulickDivision of Molecular Cardiovascular Biology, The Heart Institute Cincinnati Children's Hospital, Cincinnati, OH.
Monte S WillisDepartment of Pathology & Laboratory Medicine, University of North Carolina, Chapel Hill, NC.
Cynthia LanderMoerae Matrix, Morristown, NJ.
Jeffrey RobbinsDivision of Molecular Cardiovascular Biology, The Heart Institute Cincinnati Children's Hospital, Cincinnati, OH jeff.robbins@cchmc.org.
Cincinnati Children's Hospital Medical Center · USChildren's Hospital of Wisconsin · USMoerae Matrix (United States) · USUniversity of North Carolina at Chapel Hill · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCardiac stress can trigger production of a 40-kDa peptide fragment derived from the amino terminus of the cardiac myosin-binding protein C. Cardiac stress, as well as cMyBP-C mutations, can trigger production of 1 such truncated protein fragment, a 40-kDa peptide fragment derived from the amino terminus of cMyBP-C. Genetic expression of this 40-kDa fragment in mouse cardiomyocytes (cMyBP-C METHODS AND

resultsNontransgenic and cMyBP-C

conclusionsPharmaceutical inhibition of mitogen-activated protein kinase--activated protein kinase-2 signaling via MMI-0100 treatment is beneficial in the context of fibrotic cMyBPC

Indexed as

ActinsAnimalsCardiomyopathiesCarrier ProteinsCell DifferentiationCells, CulturedDisease Models, AnimalFibroblastsFibrosisHypertrophy, Left VentricularIntracellular Signaling Peptides and ProteinsMAP-Kinase-Activated Kinase 2Mice, Inbred C57BLMice, TransgenicMyocytes, CardiacMyosin Binding Protein CActa2 protein, mouseActinsCarrier ProteinsIntracellular Signaling Peptides and ProteinsMAP-Kinase-Activated Kinase 2MMI-0100Myosin Binding Protein CPeptidesProtein Kinase InhibitorsProtein Serine-Threonine Kinasesfibrosishypertrophy/remodelingtransgenic micetransgenic model

Identifiers

PMID28871043
PMCPMC5634300
OpenAlexW2751809384

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.