Evidence map›Paper›PMID 35317048›Full record

ArticleMolecular therapy. Methods & clinical development2022

Follistatin-like 1 promotes proliferation of matured human hypoxic iPSC-cardiomyocytes and is secreted by cardiac fibroblasts.

Marijn C Peters, Sofia Di Martino, Thomas Boelens, Jiabin Qin, Alain van Mil, Pieter A Doevendans, Steven A J Chamuleau, Joost P G Sluijter, Klaus Neef

Open access · goldAbstract read
In one paragraph

Article in Molecular therapy. Methods & clinical development, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

15 citing papers in PubMed, 19 citations in OpenAlex.

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  15. Hypo-glycosylated follistatin-like 1 for new cardiomyocyte formation.Molecular therapy. Methods & clinical development · 2022
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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

9 authors at 1 institution in 1 country.

Marijn C PetersDepartment of Cardiology, Laboratory of Experimental Cardiology, Regenerative Medicine Centre Utrecht, University Medical Centre Utrecht, University Utrecht, 3584 CX Utrecht, the Netherlands.
Sofia Di MartinoDepartment of Cardiology, Laboratory of Experimental Cardiology, Regenerative Medicine Centre Utrecht, University Medical Centre Utrecht, University Utrecht, 3584 CX Utrecht, the Netherlands.
Thomas BoelensDepartment of Cardiology, Laboratory of Experimental Cardiology, Regenerative Medicine Centre Utrecht, University Medical Centre Utrecht, University Utrecht, 3584 CX Utrecht, the Netherlands.
Jiabin QinDepartment of Cardiology, Laboratory of Experimental Cardiology, Regenerative Medicine Centre Utrecht, University Medical Centre Utrecht, University Utrecht, 3584 CX Utrecht, the Netherlands.
Alain van MilDepartment of Cardiology, Laboratory of Experimental Cardiology, Regenerative Medicine Centre Utrecht, University Medical Centre Utrecht, University Utrecht, 3584 CX Utrecht, the Netherlands.
Pieter A DoevendansDepartment of Cardiology, Laboratory of Experimental Cardiology, Regenerative Medicine Centre Utrecht, University Medical Centre Utrecht, University Utrecht, 3584 CX Utrecht, the Netherlands.
Steven A J ChamuleauDepartment of Cardiology, Laboratory of Experimental Cardiology, Regenerative Medicine Centre Utrecht, University Medical Centre Utrecht, University Utrecht, 3584 CX Utrecht, the Netherlands.
Joost P G SluijterDepartment of Cardiology, Laboratory of Experimental Cardiology, Regenerative Medicine Centre Utrecht, University Medical Centre Utrecht, University Utrecht, 3584 CX Utrecht, the Netherlands.
Klaus NeefDepartment of Cardiology, Laboratory of Experimental Cardiology, Regenerative Medicine Centre Utrecht, University Medical Centre Utrecht, University Utrecht, 3584 CX Utrecht, the Netherlands.
Utrecht University · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The human heart has limited regenerative capacity. Therefore, patients often progress to heart failure after ischemic injury, despite advances in reperfusion therapies generally decreasing mortality. Depending on its glycosylation state, Follistatin-like 1 (FSTL1) has been shown to increase cardiomyocyte (CM) proliferation, decrease CM apoptosis, and prevent cardiac rupture in animal models of ischemic heart disease. To explore its therapeutic potential, we used a human

Indexed as

fibroblastsFollistatin-like 1hypoxiaiPSC-cardiomyocytesischemic heart disease

Identifiers

PMID35317048
PMCPMC8917270
OpenAlexW4213027919

What OpenQuestion holds

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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.