Evidence map›Paper›PMID 33694131›Full record

ReviewCurrent cardiology reports2021

Understanding Heart Field Progenitor Cells for Modeling Congenital Heart Diseases.

Matthew Miyamoto, Harshi Gangrade, Emmanouil Tampakakis

Abstract readReview
PubMed Publisher
In one paragraph

Review in Current cardiology reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.6field-weighted citation impact, top 34% 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

6 citing papers in PubMed, 9 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Noncanonical Notch signals have opposing roles during cardiac development.Biochemical and biophysical research communications · 2021
    Article
  6. Heart organoids and tissue models for modeling development and disease.Seminars in cell & developmental biology · 2021
    Review
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

3 authors at 1 institution in 1 country.

Matthew MiyamotoDepartment of Medicine, Division of Cardiology, Johns Hopkins University, 720 Rutland Avenue, Ross 835, Baltimore, MD, 21205, USA.
Harshi GangradeDepartment of Medicine, Division of Cardiology, Johns Hopkins University, 720 Rutland Avenue, Ross 835, Baltimore, MD, 21205, USA.
Emmanouil TampakakisDepartment of Medicine, Division of Cardiology, Johns Hopkins University, 720 Rutland Avenue, Ross 835, Baltimore, MD, 21205, USA. etampak1@jhmi.edu.ORCID http://orcid.org/0000-0003-3143-6459
Johns Hopkins University · US

Funding

Engineering a power switch to study the contribution of stem cell-derived cardiomyocytes on heart regenerationK08HL145135 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI TAMPAKAKIS, EMMANOUIL · 2019 to 2023
$859k
NHLBI NIH HHS HL-145135NHLBI NIH HHS K08 HL145135
6 · The paper itself

Abstract

purpose of reviewHeart development is a meticulously coordinated process that involves the specification of two distinct populations of cardiac progenitor cells, namely the first and the second heart field. Disruption of heart field progenitors can result in congenital heart defects. In this review, we aim to describe the signaling pathways and transcription factors that link heart field development and congenital heart disease. RECENT

findingsSingle-cell transcriptomics, lineage-tracing mouse models, and stem cell-based in vitro modeling of cardiogenesis have significantly improved the spatiotemporal characterization of cardiac progenitors. Additionally, novel functional genomic studies have now linked more genetic variants with congenital heart disease. Dysregulation of cardiac progenitor cells causes malformations that can be lethal. Ongoing research will continue to shed light on cardiac morphogenesis and help us better understand and treat patients with congenital heart disease.

Indexed as

HeartHeart Defects, CongenitalAnimalsHumansMiceMyocardiumSignal TransductionStem CellsCardiac progenitorsCongenital heart diseaseGenetic variantsHeart defectsHeart developmentHeart fields

Identifiers

PMID33694131
OpenAlexW3135771135

What OpenQuestion holds

Textmetadata
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.