Evidence map›Paper›PMID 35867287›Full record

ReviewHeart failure reviews2022

Follistatin-like 1 and its paralogs in heart development and cardiovascular disease.

Martin Horak, DeLisa Fairweather, Piia Kokkonen, David Bednar, Julie Bienertova-Vasku

Open access · greenAbstract readReview
In one paragraph

Review in Heart failure reviews, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.8field-weighted citation impact, top 14% 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

16 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Journal of the American Heart Association · 2026
    Article
  5. Review
  6. Article
  7. Biomedicines · 2025
    Article
  8. Article
  9. Review
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  11. Article
  12. Article
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  14. Review
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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

5 authors at 2 institutions in 2 countries.

Martin HorakDepartment of Pathological Physiology, Faculty of Medicine, Masaryk University, Kamenice 5, Brno, 625 00, Czech Republic.
DeLisa FairweatherDepartment of Cardiovascular Medicine, Mayo Clinic, 4500 San Pablo Road, Jacksonville, FL, 32224, USA.
Piia KokkonenResearch Centre for Toxic Compounds in the Environment, Faculty of Science, Masaryk University, Kamenice 5, Brno, 625 00, Czech Republic.
David BednarResearch Centre for Toxic Compounds in the Environment, Faculty of Science, Masaryk University, Kamenice 5, Brno, 625 00, Czech Republic.
Julie Bienertova-VaskuDepartment of Pathological Physiology, Faculty of Medicine, Masaryk University, Kamenice 5, Brno, 625 00, Czech Republic. Julie.dobrovolna@med.muni.cz.ORCID 0000-0001-5327-808X
Masaryk University · CZMayo Clinic in Florida · US

Funding

Role of mitochondrial extracellular vesicles in CVB3 myocarditis by sexR01HL164520 · NHLBI · MAYO CLINIC JACKSONVILLE · PI FAIRWEATHER, DELISA · 2022 to 2025
$3.0M
Role of viral mitophagosomes in driving sex differences in myocarditisR21AI145356 · NIAID · MAYO CLINIC JACKSONVILLE · PI FAIRWEATHER, DELISA, SIN, JON · 2019 to 2020
$463k
Adipose-derived biogenic nanoparticles for treatment of myocarditis/DCM(MPDPI)R21AI152318 · NIAID · MAYO CLINIC JACKSONVILLE · PI FAIRWEATHER, DELISA, WOLFRAM, JOY · 2020 to 2021
$430k
Sex differences in exercise-induced mitochondrial function during viral myocarditisR21AI154927 · NIAID · MAYO CLINIC JACKSONVILLE · PI FAIRWEATHER, DELISA · 2020 to 2021
$403k
NHLBI NIH HHS R01 HL164520NIAID NIH HHS R21 AI145356NIAID NIH HHS R21 AI152318NIAID NIH HHS R21 AI154927
6 · The paper itself

Abstract

Cardiovascular diseases (CVDs) are a group of disorders affecting the heart and blood vessels and a leading cause of death worldwide. Thus, there is a need to identify new cardiokines that may protect the heart from damage as reported in GBD 2017 Causes of Death Collaborators (2018) (The Lancet 392:1736-1788). Follistatin-like 1 (FSTL1) is a cardiokine that is highly expressed in the heart and released to the serum after cardiac injury where it is associated with CVD and predicts poor outcome. The action of FSTL1 likely depends not only on the tissue source but also post-translation modifications that are target tissue- and cell-specific. Animal studies examining the effect of FSTL1 in various models of heart disease have exploded over the past 15 years and primarily report a protective effect spanning from inhibiting inflammation via transforming growth factor, preventing remodeling and fibrosis to promoting angiogenesis and hypertrophy. A better understanding of FSTL1 and its homologs is needed to determine whether this protein could be a useful novel biomarker to predict poor outcome and death and whether it has therapeutic potential. The aim of this review is to provide a comprehensive description of the literature for this family of proteins in order to better understand their role in normal physiology and CVD.

Indexed as

Cardiovascular DiseasesFollistatin-Related ProteinsAnimalsBiomarkersFibrosisFollistatinHumansBiomarkersFollistatinFollistatin-Related ProteinsFSTL1 protein, humanFSTL1FSTL4FSTL5Heart failureInflammation

Identifiers

PMID35867287
PMCPMC11140762
OpenAlexW4286716742

What OpenQuestion holds

Textmetadata
LicenceTDM
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.