Evidence map›Paper›PMID 21809354›Full record

ArticleHepatology (Baltimore, Md.)2011

A protective antiarrhythmic role of ursodeoxycholic acid in an in vitro rat model of the cholestatic fetal heart.

Michele Miragoli, Siti H Sheikh Abdul Kadir, Mary N Sheppard, Nicoló Salvarani, Matilda Virta, Sarah Wells, Max J Lab, Viacheslav O Nikolaev, Alexey Moshkov, William M Hague and 3 more

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in Hepatology (Baltimore, Md.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed, 1 pooled it
2.4field-weighted citation impact, top 11% 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

40 citing papers in PubMed, 1 synthesis or guideline pooled it, 91 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Article
  5. Review
  6. Intrahepatic cholestasis of pregnancy.Nature reviews. Disease primers · 2025
    Review
  7. Review
  8. Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Guidelines for assessment of cardiac electrophysiology and arrhythmias in small animals.American journal of physiology. Heart and circulatory physiology · 2022
    Review
  16. Article
  17. Review
  18. Pathogenic Mechanisms Underlying Cirrhotic Cardiomyopathy.Frontiers in network physiology · 2022
    Review
  19. Article
  20. Review
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

13 authors at 5 institutions in 4 countries.

Michele MiragoliNational Heart and Lung Institute, Imperial College London, London, England.
Siti H Sheikh Abdul Kadir
Mary N Sheppard
Nicoló Salvarani
Matilda Virta
Sarah Wells
Max J Lab
Viacheslav O Nikolaev
Alexey Moshkov
William M Hague
Stephan Rohr
Catherine Williamson
Julia Gorelik
Lung Institute · USImperial College London · GBUniversity of Bern · CHRoyal Brompton Hospital · GBUniversity of Adelaide · AU

Funding

Wellcome Trust 090594
6 · The paper itself

Abstract

unlabelledIntrahepatic cholestasis of pregnancy may be complicated by fetal arrhythmia, fetal hypoxia, preterm labor, and, in severe cases, intrauterine death. The precise etiology of fetal death is not known. However, taurocholate has been demonstrated to cause arrhythmia and abnormal calcium dynamics in cardiomyocytes. To identify the underlying reason for increased susceptibility of fetal cardiomyocytes to arrhythmia, we studied myofibroblasts (MFBs), which appear during structural remodeling of the adult diseased heart. In vitro, they depolarize rat cardiomyocytes via heterocellular gap junctional coupling. Recently, it has been hypothesized that ventricular MFBs might appear in the developing human heart, triggered by physiological fetal hypoxia. However, their presence in the fetal heart (FH) and their proarrhythmogenic effects have not been systematically characterized. Immunohistochemistry demonstrated that ventricular MFBs transiently appear in the human FH during gestation. We established two in vitro models of the maternal heart (MH) and FH, both exposed to increasing doses of taurocholate. The MH model consisted of confluent strands of rat cardiomyocytes, whereas for the FH model, we added cardiac MFBs on top of cardiomyocytes. Taurocholate in the FH model, but not in the MH model, slowed conduction velocity from 19 to 9 cm/s, induced early after depolarizations, and resulted in sustained re-entrant arrhythmias. These arrhythmic events were prevented by ursodeoxycholic acid, which hyperpolarized MFB membrane potential by modulating potassium conductance.

conclusionThese results illustrate that the appearance of MFBs in the FH may contribute to arrhythmias. The above-described mechanism represents a new therapeutic approach for cardiac arrhythmias at the level of MFB.

Indexed as

AdultAnimalsAnti-Arrhythmia AgentsArrhythmias, CardiacCells, CulturedCholestasis, IntrahepaticDisease Models, AnimalFemaleFetal HeartHeart VentriclesHumansIn Vitro TechniquesMuscle CellsPregnancyPregnancy ComplicationsRatsAnti-Arrhythmia AgentsUrsodeoxycholic Acid

Identifiers

PMID21809354
PMCPMC4900448
OpenAlexW1985056901

What Socratic 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 Socratic graph.