Evidence map›Paper›PMID 34689154›Full record

ArticleCell death discovery2021

Fortilin inhibits p53, halts cardiomyocyte apoptosis, and protects the heart against heart failure.

Preedakorn Chunhacha, Decha Pinkaew, Patuma Sinthujaroen, Dawn E Bowles, Ken Fujise

Open access · goldAbstract read
In one paragraph

Article in Cell death discovery, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed, 1 pooled it
0.8field-weighted citation impact, top 28% 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, 1 synthesis or guideline pooled it, 18 citations in OpenAlex.

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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 4 institutions in 2 countries.

Preedakorn Chunhacha *Division of Cardiology, Department of Medicine, University of Washington, Seattle, WA, 98109, USA.
Decha Pinkaew *Division of Cardiology, Department of Medicine, University of Washington, Seattle, WA, 98109, USA.ORCID http://orcid.org/0000-0001-8334-1545
Patuma SinthujaroenDivision of Cardiology, Department of Medicine, University of Washington, Seattle, WA, 98109, USA.ORCID http://orcid.org/0000-0002-0483-1755
Dawn E BowlesDivision of Surgical Sciences, Department of Surgery, Duke University, Durham, NC, 27710, USA.
Ken FujiseDivision of Cardiology, Department of Medicine, University of Washington, Seattle, WA, 98109, USA. kfujise@uw.edu.ORCID http://orcid.org/0000-0002-6763-8055
University of Washington · USChulalongkorn University · THDuke University · USPrince of Songkla University · TH

Funding

Fortilin, p53, and atherosclerosisR01HL117247 · NHLBI · UNIVERSITY OF WASHINGTON · PI CHEN, SHIYOU, FUJISE, KEN · 2013 to 2023
$4.7M
Fortilin, CTNNA3, and the HeartR01HL152723 · NHLBI · UNIVERSITY OF WASHINGTON · PI FUJISE, KEN · 2021 to 2024
$2.7M
USING FORTILIN INHIBITORS TO BLOCK ATHEROSCLEROSISR01HL138992 · NHLBI · UNIVERSITY OF WASHINGTON · PI FUJISE, KEN, SRIVASTAVA, SANJAY · 2017 to 2020
$2.6M
Gut Dysbiosis and Cardiac Remodeling in IBDR01HL152683 · NHLBI · UNIVERSITY OF TEXAS MED BR GALVESTON · PI FUJISE, KEN, LI, QINGJIE · 2020 to 2023
$2.6M
Characterization of Fortilin, A Novel Anti-p53 ProteinR01HL068024 · NHLBI · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI FUJISE, KEN · 2001 to 2005
$992k
NHLBI NIH HHS R01 HL068024NHLBI NIH HHS R01 HL117247NHLBI NIH HHS R01 HL138992NHLBI NIH HHS R01 HL152683NHLBI NIH HHS R01 HL152723U.S. Department of Health & Human Services | National Institutes of Health (NIH) HL117247U.S. Department of Health & Human Services | National Institutes of Health (NIH) HL138992U.S. Department of Health & Human Services | National Institutes of Health (NIH) HL152723
6 · The paper itself

Abstract

Heart failure (HF) has reached epidemic proportions in developed countries, affecting over 20 million people worldwide. Despite modern medical and device therapies, 60-70% of HF patients still die within 5 years of diagnosis as it relentlessly progresses through pervasive apoptotic loss of cardiomyocytes. Although fortilin, a 172-amino-acid anti-p53 molecule, is one of the most expressed proteins in the heart, its precise role there has remained unknown. Also unclear is how cardiomyocytes are protected against apoptosis. Here, we report that failing human hearts express less fortilin than do non-failing hearts. We also found that mice lacking fortilin in the heart (fortilin

Identifiers

PMID34689154
PMCPMC8542040
OpenAlexW3208393369

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.