Evidence map›Paper›PMID 29358198›Full record

ArticleJournal of the American Heart Association2018

Transplantation of Allogeneic Pericytes Improves Myocardial Vascularization and Reduces Interstitial Fibrosis in a Swine Model of Reperfused Acute Myocardial Infarction.

Valeria Vincenza Alvino, Rodrigo Fernández-Jiménez, Iker Rodriguez-Arabaolaza, Sadie Slater, Giuseppe Mangialardi, Elisa Avolio, Helen Spencer, Lucy Culliford, Sakinah Hassan, Lorena Sueiro Ballesteros and 11 more

Open access · goldAbstract read
In one paragraph

Article in Journal of the American Heart Association, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
4.8field-weighted citation impact, top 4% 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

29 citing papers in PubMed, 53 citations in OpenAlex.

  1. Review
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  5. Intramyocardial immunomodulation with human CD16Frontiers in cardiovascular medicine · 2024
    Article
  6. A perspective on Notch signalling in progression and arrhythmogenesis in familial hypertrophic and dilated cardiomyopathies.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2023
    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

21 authors at 6 institutions in 4 countries.

Valeria Vincenza AlvinoBristol Heart Institute, School of Clinical Sciences, University of Bristol, United Kingdom.
Rodrigo Fernández-JiménezCentro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC), Madrid, Spain.
Iker Rodriguez-ArabaolazaBristol Heart Institute, School of Clinical Sciences, University of Bristol, United Kingdom.
Sadie SlaterBristol Heart Institute, School of Clinical Sciences, University of Bristol, United Kingdom.
Giuseppe MangialardiBristol Heart Institute, School of Clinical Sciences, University of Bristol, United Kingdom.
Elisa AvolioBristol Heart Institute, School of Clinical Sciences, University of Bristol, United Kingdom.
Helen SpencerBristol Heart Institute, School of Clinical Sciences, University of Bristol, United Kingdom.
Lucy CullifordBristol Heart Institute, School of Clinical Sciences, University of Bristol, United Kingdom.
Sakinah HassanBristol Heart Institute, School of Clinical Sciences, University of Bristol, United Kingdom.
Lorena Sueiro BallesterosSchool of Cellular and Molecular Medicine, University of Bristol, United Kingdom.
Andrew HermanSchool of Cellular and Molecular Medicine, University of Bristol, United Kingdom.
Ali Ayaon-AlbarránCentro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC), Madrid, Spain.
Carlos Galán-ArriolaCentro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC), Madrid, Spain.
Javier Sánchez-GonzálezPhilips Healthcare, Madrid, Spain.
Helena HennesseyBristol Genetics Laboratory, Southmead Hospital, Bristol, United Kingdom.
Catherine DelmegeBristol Genetics Laboratory, Southmead Hospital, Bristol, United Kingdom.
Raimondo AscioneBristol Heart Institute, School of Clinical Sciences, University of Bristol, United Kingdom.
Costanza EmanueliBristol Heart Institute, School of Clinical Sciences, University of Bristol, United Kingdom.
Gianni Davide AngeliniBristol Heart Institute, School of Clinical Sciences, University of Bristol, United Kingdom.
Borja IbanezCentro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC), Madrid, Spain mdprm@bristol.ac.uk bibanez@cnic.es.
Paolo MadedduBristol Heart Institute, School of Clinical Sciences, University of Bristol, United Kingdom mdprm@bristol.ac.uk bibanez@cnic.es.
University of Bristol · GBNIHR Bristol Cardiovascular Biomedical Research Unit · GBSpanish National Centre for Cardiovascular Research · ESSouthmead Hospital · GBCentro de Investigación en Red en Enfermedades Cardiovasculares · ESPhilips (Spain) · ES

Funding

British Heart Foundation CH/1992027/7163British Heart Foundation FS/16/64/32480British Heart Foundation PG/07/046/22772British Heart Foundation PG/10/81/28606British Heart Foundation SP/12/7/29572Department of HealthMedical Research Council MR/L012723/1
6 · The paper itself

Abstract

backgroundTransplantation of adventitial pericytes (APCs) promotes cardiac repair in murine models of myocardial infarction. The aim of present study was to confirm the benefit of APC therapy in a large animal model. METHODS AND

resultsWe performed a blind, randomized, placebo-controlled APC therapy trial in a swine model of reperfused myocardial infarction. A first study used human APCs (hAPCs) from patients undergoing coronary artery bypass graft surgery. A second study used allogeneic swine APCs (sAPCs). Primary end points were (1) ejection fraction as assessed by cardiac magnetic resonance imaging and (2) myocardial vascularization and fibrosis as determined by immunohistochemistry. Transplantation of hAPCs reduced fibrosis but failed to improve the other efficacy end points. Incompatibility of the xenogeneic model was suggested by the occurrence of a cytotoxic response following in vitro challenge of hAPCs with swine spleen lymphocytes and the failure to retrieve hAPCs in transplanted hearts. We next considered sAPCs as an alternative. Flow cytometry, immunocytochemistry, and functional/cytotoxic assays indicate that sAPCs are a surrogate of hAPCs. Transplantation of allogeneic sAPCs benefited capillary density and fibrosis but did not improve cardiac magnetic resonance imaging indices of contractility. Transplanted cells were detected in the border zone.

conclusionsImmunologic barriers limit the applicability of a xenogeneic swine model to assess hAPC efficacy. On the other hand, we newly show that transplantation of allogeneic sAPCs is feasible, safe, and immunologically acceptable. The approach induces proangiogenic and antifibrotic benefits, though these effects were not enough to result in functional improvements.

Indexed as

Neovascularization, PhysiologicVentricular Function, LeftVentricular RemodelingAgedAged, 80 and overAllogeneic CellsAnimalsCell- and Tissue-Based TherapyCells, CulturedDisease Models, AnimalFemaleFibrosisHeterograftsHumansMaleMiddle Agedangiogenesiscell therapylarge animal modelsmyocardial infarctionpericytes

Identifiers

PMID29358198
PMCPMC5850145
OpenAlexW2792969825

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.