Evidence map›Paper›PMID 31801200›Full record

ArticleInternational journal of molecular sciences2019

Phenotypic Screen with the Human Secretome Identifies FGF16 as Inducing Proliferation of iPSC-Derived Cardiac Progenitor Cells.

Karin Jennbacken, Fredrik Wågberg, Ulla Karlsson, Jerry Eriksson, Lisa Magnusson, Marjorie Chimienti, Piero Ricchiuto, Jenny Bernström, Mei Ding, Douglas Ross-Thriepland and 10 more

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.0field-weighted citation impact, top 23% 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

13 citing papers in PubMed, 25 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Advances in Drug Discovery for Cardiomyocyte Proliferation.Current treatment options in cardiovascular medicine · 2025
    Review
  5. The molecular mechanisms of cardiac development and related diseases.Signal transduction and targeted therapy · 2024
    Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. Review
  12. Secretome-Based Screening in Target Discovery.SLAS discovery : advancing life sciences R & D · 2020
    Review
  13. 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

20 authors at 4 institutions in 2 countries.

Karin JennbackenBioscience Cardiovascular, Research and Early Development, Cardiovascular, Renal and Metabolism, BioPharmaceutical R&D, AstraZeneca, Gothenburg, 43150 Mölndal, Sweden.
Fredrik WågbergMechanistic Biology and Profiling, Discovery Sciences, R&D, AstraZeneca, Gothenburg, 43150 Mölndal, Sweden.
Ulla KarlssonMechanistic Biology and Profiling, Discovery Sciences, R&D, AstraZeneca, Gothenburg, 43150 Mölndal, Sweden.
Jerry ErikssonBioscience Cardiovascular, Research and Early Development, Cardiovascular, Renal and Metabolism, BioPharmaceutical R&D, AstraZeneca, Gothenburg, 43150 Mölndal, Sweden.
Lisa MagnussonBioscience Cardiovascular, Research and Early Development, Cardiovascular, Renal and Metabolism, BioPharmaceutical R&D, AstraZeneca, Gothenburg, 43150 Mölndal, Sweden.
Marjorie ChimientiBioscience Cardiovascular, Research and Early Development, Cardiovascular, Renal and Metabolism, BioPharmaceutical R&D, AstraZeneca, Gothenburg, 43150 Mölndal, Sweden.
Piero RicchiutoQuantitative Biology, Discovery Sciences, R&D, AstraZeneca, Cambridge CB40WG, UK.
Jenny BernströmDiscovery Biology, Discovery Sciences, R&D, AstraZeneca, Gothenburg, 43150 Mölndal, Sweden.
Mei DingDiscovery Biology, Discovery Sciences, R&D, AstraZeneca, Gothenburg, 43150 Mölndal, Sweden.
Douglas Ross-ThrieplandDiscovery Biology, Discovery Sciences, R&D, AstraZeneca, Cambridge CB40WG, UK.
Yafeng XueStructure and Biophysics and Fragment screening, Discovery Sciences, R&D, AstraZeneca, Gothenburg, 43150 Mölndal, Sweden.
Diluka PeirisAttana AB, 11419 Stockholm, Sweden.
Teodor AastrupAttana AB, 11419 Stockholm, Sweden.
Hanna TegelDepartment of Protein Science, School of engineering Sciences in Chemistry, Biotechnology and Health, KTH-Royal Institute of Technology, 11421 Stockholm, Sweden.ORCID 0000-0002-7067-9173
Sophia HoberDepartment of Protein Science, School of engineering Sciences in Chemistry, Biotechnology and Health, KTH-Royal Institute of Technology, 11421 Stockholm, Sweden.
Åsa SivertssonDepartment of Protein Science, School of engineering Sciences in Chemistry, Biotechnology and Health, KTH-Royal Institute of Technology, 11421 Stockholm, Sweden.
Mathias UhlénDepartment of Protein Science, School of engineering Sciences in Chemistry, Biotechnology and Health, KTH-Royal Institute of Technology, 11421 Stockholm, Sweden.ORCID 0000-0002-4858-8056
Per-Erik StrömstedtMechanistic Biology and Profiling, Discovery Sciences, R&D, AstraZeneca, Gothenburg, 43150 Mölndal, Sweden.
Rick DaviesDiscovery Biology, Discovery Sciences, R&D, AstraZeneca, Cambridge CB40WG, UK.
Lovisa Holmberg SchiavoneDiscovery Biology, Discovery Sciences, R&D, AstraZeneca, Gothenburg, 43150 Mölndal, Sweden.ORCID 0000-0001-8496-0444
AstraZeneca (Sweden) · SEKTH Royal Institute of Technology · SEAstraZeneca (United Kingdom) · GBAttana (Sweden) · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Paracrine factors can induce cardiac regeneration and repair post myocardial infarction by stimulating proliferation of cardiac cells and inducing the anti-fibrotic, antiapoptotic, and immunomodulatory effects of angiogenesis. Here, we screened a human secretome library, consisting of 923 growth factors, cytokines, and proteins with unknown function, in a phenotypic screen with human cardiac progenitor cells. The primary readout in the screen was proliferation measured by nuclear count. From this screen, we identified FGF1, FGF4, FGF9, FGF16, FGF18, and seven additional proteins that induce proliferation of cardiac progenitor cells. FGF9 and FGF16 belong to the same FGF subfamily, share high sequence identity, and are described to have similar receptor preferences. Interestingly, FGF16 was shown to be specific for proliferation of cardiac progenitor cells, whereas FGF9 also proliferated human cardiac fibroblasts. Biosensor analysis of receptor preferences and quantification of receptor abundances suggested that FGF16 and FGF9 bind to different FGF receptors on the cardiac progenitor cells and cardiac fibroblasts. FGF16 also proliferated naïve cardiac progenitor cells isolated from mouse heart and human cardiomyocytes derived from induced pluripotent cells. Taken together, the data suggest that FGF16 could be a suitable paracrine factor to induce cardiac regeneration and repair.

Indexed as

AnimalsCell DifferentiationCell ProliferationCHO CellsCricetulusFemaleFibroblast Growth FactorsFibroblastsGene ExpressionGene LibraryHigh-Throughput Screening AssaysHumansInduced Pluripotent Stem CellsMiceMice, Inbred C57BLMyocytes, CardiacFGF16 protein, humanFibroblast Growth Factorscardiac progenitor cellsfibroblast growth factor 16fibroblast growth factorshuman secretomephenotypic screening

Identifiers

PMID31801200
PMCPMC6928864
OpenAlexW2989874401

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.