Evidence map›Paper›PMID 24670798›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2014

Congenital heart disease linked to maternal autoimmunity against cardiac myosin.

Charles R Cole, Katherine E Yutzey, Anoop K Brar, Lisa S Goessling, Sarah J Van Vickle-Chavez, Madeleine W Cunningham, Pirooz Eghtesady

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.2field-weighted citation impact, top 20% 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

6 citing papers in PubMed, 24 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

7 authors at 4 institutions in 1 country.

Charles R ColeDivision of Molecular Cardiovascular Biology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 45229;
Katherine E Yutzey
Anoop K Brar
Lisa S Goessling
Sarah J Van Vickle-Chavez
Madeleine W Cunningham
Pirooz Eghtesady
Washington University in St. Louis · USCincinnati Children's Hospital Medical Center · USUniversity of Oklahoma Health Sciences Center · USWashington University Medical Center · US

Funding

AUTOIMMUNE DETERMINANTS OF HUMAN CARDIAC MYOSINR01HL056267 · NHLBI · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI COOPER, LESLIE T, CUNNINGHAM, MADELEINE W. · 1997 to 2013
$4.7M
MYOSIN--A LINK BETWEEN STREPTOCOCCI AND HEARTR37HL035280 · NHLBI · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI CUNNINGHAM, MADELEINE W. · 1999 to 2008
$3.0M
Autoimmune Determinants of Human Cardiac MyosinR56HL056267 · NHLBI · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI COOPER, LESLIE T, CUNNINGHAM, MADELEINE W. · 2008 to 2015
$933k
Developing an animal model of HLHS: role of immune mediated injuryR21HL104391 · NHLBI · WASHINGTON UNIVERSITY · PI EGHTESADY, PIROOZ · 2011 to 2012
$416k
Myocardial Protection during Fetal Bypass: Role of Calcium CyclingF32HL103054 · NHLBI · CINCINNATI CHILDRENS HOSP MED CTR · PI COLE, CHARLES R · 2010 to 2011
$107k
NHLBI NIH HHS F32 HL103054NHLBI NIH HHS F32-HL103054NHLBI NIH HHS R01 HL056267NHLBI NIH HHS R01-HL56267NHLBI NIH HHS R21 HL104391NHLBI NIH HHS R21-HL104391NHLBI NIH HHS R37 HL035280NHLBI NIH HHS R37-HL35280NHLBI NIH HHS R56 HL056267
6 · The paper itself

Abstract

Structural congenital heart disease (CHD) has not previously been linked to autoimmunity. In our study, we developed an autoimmune model of structural CHD that resembles hypoplastic left heart syndrome (HLHS), a life-threatening CHD primarily affecting the left ventricle. Because cardiac myosin (CM) is a dominant autoantigen in autoimmune heart disease, we hypothesized that immunization with CM might lead to transplacental passage of maternal autoantibodies and a prenatal HLHS phenotype in exposed fetuses. Elevated anti-CM autoantibodies in maternal and fetal sera, as well as IgG reactivity in fetal myocardium, were correlated with structural CHD that included diminished left ventricular cavity dimensions in the affected progeny. Further, fetuses that developed a marked HLHS phenotype had elevated serum titers of anti-β-adrenergic receptor Abs, as well as increased protein kinase A activity, suggesting a potential mechanism for the observed pathological changes. Our maternal-fetal model presents a new concept linking autoimmunity against CM and cardiomyocyte proliferation with cardinal features of HLHS. To our knowledge, this report shows the first evidence in support of a novel immune-mediated mechanism for pathogenesis of structural CHD that may have implications in its future diagnosis and treatment.

Indexed as

AnimalsAutoantibodiesAutoimmunityBlotting, WesternCardiac MyosinsDisease Models, AnimalEnzyme-Linked Immunosorbent AssayFemaleHeart Defects, CongenitalHypoplastic Left Heart SyndromeImmunohistochemistryRatsRats, Inbred LewAutoantibodiesCardiac Myosins

Identifiers

PMID24670798
PMCPMC4130707
OpenAlexW1634920420

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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.