Evidence map›Paper›PMID 24278323›Full record

ArticlePloS one2013

Loss of the cytoskeletal protein Pdlim7 predisposes mice to heart defects and hemostatic dysfunction.

Jennifer Krcmery, Rajesh Gupta, Rudyard W Sadleir, Molly J Ahrens, Sol Misener, Christine Kamide, Philip Fitchev, Douglas W Losordo, Susan E Crawford, Hans-Georg Simon

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.7field-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, 19 citations in OpenAlex.

  1. AClinical case reports · 2025
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  3. Proximity proteomics of synaptopodin provides insight into the molecular composition of the spine apparatus of dendritic spines.Proceedings of the National Academy of Sciences of the United States of America · 2022
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  4. The unexpected versatility of ALP/Enigma family proteins.Frontiers in cell and developmental biology · 2022
    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

10 authors at 3 institutions in 1 country.

Jennifer KrcmeryDepartment of Pediatrics, Feinberg School of Medicine, Northwestern University, Chicago, Illinois, United States of America ; Ann and Robert H. Lurie Children's Hospital of Chicago Research Center, Chicago, Illinois, United States of America.
Rajesh Gupta
Rudyard W Sadleir
Molly J Ahrens
Sol Misener
Christine Kamide
Philip Fitchev
Douglas W Losordo
Susan E Crawford
Hans-Georg Simon
Northwestern University · USLurie Children's Hospital · USSaint Louis University · US

Funding

Heart development following genetic inactivation of Lmp4F31HL090031 · NHLBI · LURIE CHILDREN'S HOSPITAL OF CHICAGO · PI KRCMERY, JENNIFER K · 2007 to 2011
$145k
NHLBI NIH HHS F31 HL090031NHLBI NIH HHS F31HL090031
6 · The paper itself

Abstract

The actin-associated protein Pdlim7 is essential for heart and fin development in zebrafish; however, the expression and function of this PDZ-LIM family member in the mammal has remained unclear. Here, we show that Pdlim7 predominantly localizes to actin-rich structures in mice including the heart, vascular smooth muscle, and platelets. To test the requirement for Pdlim7 in mammalian development and function, we analyzed a mouse strain with global genetic inactivation of Pdlim7. We demonstrate that Pdlim7 loss-of-function leads to significant postnatal mortality. Inactivation of Pdlim7 does not disrupt cardiac development, but causes mild cardiac dysfunction in adult mice. Adult Pdlim7(-/-) mice displayed increased mitral and tricuspid valve annulus to body weight ratios. These structural aberrations in Pdlim7(-/-) mice were supported by three-dimensional reconstructions of adult cardiac valves, which revealed increased surface area to volume ratios for the mitral and tricuspid valve leaflets. Unexpectedly, we found that loss of Pdlim7 triggers systemic venous and arterial thrombosis, leading to significant mortality shortly after birth in Pdlim7(+/-) (11/60) and Pdlim7(-/-) (19/35) mice. In line with a prothrombotic phenotype, adult Pdlim7(-/-) mice exhibit dramatically decreased tail bleed times compared to controls. These findings reveal a novel and unexpected function for Pdlim7 in maintaining proper hemostasis in neonatal and adult mice.

Indexed as

HemostasisActinsAgingAnimalsBlood Cell CountBlood PlateletsCrosses, GeneticCytoskeletal ProteinsEmbryonic DevelopmentFemaleHeartHeart Defects, CongenitalHeart ValvesHeterozygoteIntracellular Signaling Peptides and ProteinsLIM Domain ProteinsActinsCytoskeletal ProteinsIntracellular Signaling Peptides and ProteinsLIM Domain ProteinsPdlim7 protein, mouse

Identifiers

PMID24278323
PMCPMC3835322
OpenAlexW2071801990

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.