Evidence map›Paper›PMID 29402309›Full record

ArticleStem cell research & therapy2018

Embryonic stem cell-derived cardiomyocytes for the treatment of doxorubicin-induced cardiomyopathy.

Danúbia Silva Dos Santos, Guilherme Visconde Brasil, Isalira Peroba Rezende Ramos, Fernanda Cristina Paccola Mesquita, Tais Hanae Kasai-Brunswick, Michelle Lopes Araújo Christie, Gustavo Monnerat Cahli, Raiana Andrade Quintanilha Barbosa, Sandro Torrentes da Cunha, Jonathas Xavier Pereira and 4 more

Open access · goldAbstract read
In one paragraph

Article in Stem cell research & therapy, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing 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

11 citing papers in PubMed, 19 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

14 authors at 4 institutions in 1 country.

Danúbia Silva Dos SantosInstituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Av. Carlos Chagas Filho 373 Bloco G-Sala G2-053, Rio de Janeiro, RJ, 21941-902, Brazil.
Guilherme Visconde BrasilInstituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Av. Carlos Chagas Filho 373 Bloco G-Sala G2-053, Rio de Janeiro, RJ, 21941-902, Brazil.
Isalira Peroba Rezende RamosInstituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Av. Carlos Chagas Filho 373 Bloco G-Sala G2-053, Rio de Janeiro, RJ, 21941-902, Brazil.
Fernanda Cristina Paccola MesquitaInstituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Av. Carlos Chagas Filho 373 Bloco G-Sala G2-053, Rio de Janeiro, RJ, 21941-902, Brazil.
Tais Hanae Kasai-BrunswickInstituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Av. Carlos Chagas Filho 373 Bloco G-Sala G2-053, Rio de Janeiro, RJ, 21941-902, Brazil.
Michelle Lopes Araújo ChristieInstituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Av. Carlos Chagas Filho 373 Bloco G-Sala G2-053, Rio de Janeiro, RJ, 21941-902, Brazil.
Gustavo Monnerat CahliInstituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Av. Carlos Chagas Filho 373 Bloco G-Sala G2-053, Rio de Janeiro, RJ, 21941-902, Brazil.
Raiana Andrade Quintanilha BarbosaInstituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Av. Carlos Chagas Filho 373 Bloco G-Sala G2-053, Rio de Janeiro, RJ, 21941-902, Brazil.
Sandro Torrentes da CunhaInstituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Av. Carlos Chagas Filho 373 Bloco G-Sala G2-053, Rio de Janeiro, RJ, 21941-902, Brazil.
Jonathas Xavier PereiraDepartamento de Patologia-Faculdade de Medicina, Hospital Universitário Clementino Fraga Filho, Universiade Federal do Rio de Janeiro, Av. Rodolpho Paulo Rocco, 255, Sub-solo, SAP, Rio de Janeiro, RJ, 21910-590, Brazil.
Emiliano MedeiInstituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Av. Carlos Chagas Filho 373 Bloco G-Sala G2-053, Rio de Janeiro, RJ, 21941-902, Brazil.
Antonio Carlos Campos de CarvalhoInstituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Av. Carlos Chagas Filho 373 Bloco G-Sala G2-053, Rio de Janeiro, RJ, 21941-902, Brazil.
Adriana Bastos CarvalhoInstituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Av. Carlos Chagas Filho 373 Bloco G-Sala G2-053, Rio de Janeiro, RJ, 21941-902, Brazil.
Regina Coeli Dos Santos GoldenbergInstituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Av. Carlos Chagas Filho 373 Bloco G-Sala G2-053, Rio de Janeiro, RJ, 21941-902, Brazil. rcoeli@biof.ufrj.br.
Universidade Federal do Rio de Janeiro · BRNational Institute of Science and Technology for Structural Biology and Bioimaging · BRHospital Universitário Clementino Fraga Filho · BRNational Institute of Science and Technology in Regenerative Medicine · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDoxorubicin (Dox) is a chemotherapy drug with limited application due to cardiotoxicity that may progress to heart failure. This study aims to evaluate the role of cardiomyocytes derived from mouse embryonic stem cells (CM-mESCs) in the treatment of Dox-induced cardiomyopathy (DIC) in mice.

methodsThe mouse embryonic stem cell (mESC) line E14TG2A was characterized by karyotype analysis, gene expression using RT-PCR and immunofluorescence. Cells were transduced with luciferase 2 and submitted to cardiac differentiation. Total conditioned medium (TCM) from the CM-mESCs was collected for proteomic analysis. To establish DIC in CD1 mice, Dox (7.5 mg/kg) was administered once a week for 3 weeks, resulting in a cumulative Dox dose of 22.5 mg/kg. At the fourth week, a group of animals was injected intramyocardially with CM-mESCs (8 × 10

resultsmESCs exhibited a normal karyotype and expressed pluripotent markers. Proteomic analysis of TCM showed proteins related to the negative regulation of cell death. CM-mESCs presented ventricular action potential characteristics. Mice that received Dox developed heart failure and showed significant differences in body weight, ejection fraction (EF), end-systolic volume (ESV), stroke volume (SV), heart rate and QT and corrected QT (QTc) intervals when compared to the control group. After cell or placebo injection, the Dox + CM-mESC group showed significant increases in EF and SV when compared to the Dox + placebo group. Reduction in ESV and QT and QTc intervals in Dox + CM-mESC-treated mice was observed at 5 or 30 days after cell treatment. Cells were detected up to 11 days after injection. The Dox + CM-mESC group showed a significant reduction in the percentage of apoptotic cardiomyocytes in the hearts of mice when compared to the Dox + placebo group.

conclusionsCM-mESC transplantation improves cardiac function in mice with DIC.

Indexed as

CardiomyopathiesCell LineDoxorubicinHuman Embryonic Stem CellsHumansInduced Pluripotent Stem CellsMyocytes, CardiacDoxorubicinCardiomyocytes derived from mouse embryonic stem cellsCell therapyDox-induced cardiomyopathyHeart failure

Identifiers

PMID29402309
PMCPMC5799903
OpenAlexW2796883284

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.