Evidence map›Paper›PMID 25268137›Full record

ArticlePloS one2014

Abnormal calcium handling and exaggerated cardiac dysfunction in mice with defective vitamin d signaling.

Sangita Choudhury, Soochan Bae, Qingen Ke, Ji Yoo Lee, Sylvia S Singh, René St-Arnaud, Federica Del Monte, Peter M Kang

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 2 pooled it
1.3field-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

15 citing papers in PubMed, 2 syntheses or guidelines pooled it, 23 citations in OpenAlex.

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  14. Vitamin D, reactive oxygen species and calcium signalling in ageing and disease.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2016
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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

8 authors at 2 institutions in 2 countries.

Sangita ChoudhuryCardiovascular Institute, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts, United States of America.
Soochan BaeCardiovascular Institute, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts, United States of America.
Qingen KeCardiovascular Institute, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts, United States of America.
Ji Yoo LeeCardiovascular Institute, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts, United States of America.
Sylvia S SinghCardiovascular Institute, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts, United States of America.
René St-ArnaudShriners Hospital and Departments of Surgery and Human Genetics, McGill University, Montreal, Canada.
Federica Del MonteCardiovascular Institute, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts, United States of America.
Peter M KangCardiovascular Institute, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts, United States of America.
Beth Israel Deaconess Medical Center · USMcGill University · CA

Funding

PHOSPHOINOSITIDE-3 KINASE IN CARDIAC HYPERTROPHYR01HL065742 · NHLBI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI KANG, PETER M · 2000 to 2004
$3.1M
NHLBI NIH HHS R01 HL065742NHLBI NIH HHS R01 HL65742
6 · The paper itself

Abstract

aimAltered vitamin D signaling is associated with cardiac dysfunction, but the pathogenic mechanism is not clearly understood. We examine the mechanism and the role of vitamin D signaling in the development of cardiac dysfunction. METHODS AND

resultsWe analyzed 1α-hydroxylase (1α-OHase) knockout (1α-OHase-/-) mice, which lack 1α-OH enzymes that convert the inactive form to hormonally active form of vitamin D. 1α-OHase-/- mice showed modest cardiac hypertrophy at baseline. Induction of pressure overload by transverse aortic constriction (TAC) demonstrated exaggerated cardiac dysfunction in 1α-OHase-/- mice compared to their WT littermates with a significant increase in fibrosis and expression of inflammatory cytokines. Analysis of calcium (Ca2+) transient demonstrated profound Ca2+ handling abnormalities in 1α-OHase-/- mouse cardiomyocytes (CMs), and treatment with paricalcitol (PC), an activated vitamin D3 analog, significantly attenuated defective Ca2+ handling in 1α-OHase-/- CMs. We further delineated the effect of vitamin D deficiency condition to TAC by first correcting the vitamin D deficiency in 1α-OHase-/- mice, followed then by either a daily maintenance dose of vitamin D or vehicle (to achieve vitamin D deficiency) at the time of sham or TAC. In mice treated with vitamin D, there was a significant attenuation of TAC-induced cardiac hypertrophy, interstitial fibrosis, inflammatory markers, Ca2+ handling abnormalities and cardiac function compared to the vehicle treated animals.

conclusionsOur results provide insight into the mechanism of cardiac dysfunction, which is associated with severely defective Ca2+ handling and defective vitamin D signaling in 1α-OHase-/- mice.

Indexed as

Signal TransductionAnimalsAortic Valve StenosisCalciumCardiomegalyErgocalciferolsFibrosisGene Expression RegulationMaleMiceMice, Inbred C57BLMice, KnockoutMyocytes, CardiacPrimary Cell CultureSteroid HydroxylasesVitamin DCalciumErgocalciferolsparicalcitolSteroid HydroxylasesVitamin Dvitamin D 1-alpha hydroxylase

Identifiers

PMID25268137
PMCPMC4182450
OpenAlexW2123524706

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.