Evidence map›Paper›PMID 28989945›Full record

ArticleCellR4-- repair, replacement, regeneration, & reprogramming2014

The cardiac regenerative potential of myoblasts remains limited despite improving their survival via antioxidant treatment.

Sarah A Beckman, Naosumi Sekiya, William C W Chen, Logan Mlakar, Kimimassa Tobita, Johnny Huard

Open access · greenAbstract read
In one paragraph

Article in CellR4-- repair, replacement, regeneration, & reprogramming, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact, top 58% 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

0 citing papers in PubMed, 1 citations in OpenAlex.

No citing paper in PubMed yet.

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

6 authors at 1 institution in 1 country.

Sarah A BeckmanDepartment of Pathology, University of Pittsburgh, Pittsburgh, PA, U.S.A.
Naosumi SekiyaDepartment of Orthopaedic Surgery, University of Pittsburgh, Pittsburgh, PA, U.S.A.
William C W ChenDepartment of Orthopaedic Surgery, University of Pittsburgh, Pittsburgh, PA, U.S.A.
Logan MlakarStem Cell Research Center, University of Pittsburgh, Pittsburgh, PA, U.S.A.
Kimimassa TobitaDepartment of Developmental Biology, University of Pittsburgh, Pittsburgh, PA, U.S.A.
Johnny HuardDepartment of Orthopaedic Surgery, University of Pittsburgh, Pittsburgh, PA, U.S.A.
University of Pittsburgh · US

Funding

Preclinical Gene Therapy in a Large Animal Model of DMDU54AR050733 · NIAMS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI WATKINS, SIMON C · 2003 to 2008
$7.7M
Cardiovascular Bioengineering Training ProgramT32HL076124 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI SANJEEV G SHROFF · 2005 to 2026
$7.0M
NHLBI NIH HHS T32 HL076124NIAMS NIH HHS U54 AR050733
6 · The paper itself

Abstract

introductionSince myoblasts have been limited by poor cell survival after cellular myoplasty, the major goal of the current study was to determine whether improving myoblast survival with an antioxidant could improve cardiac function after the transplantation of the myoblasts into an acute myocardial infarction.

backgroundWe previously demonstrated that early myogenic progenitors such as muscle-derived stem cells (MDSCs) exhibited superior cell survival and improved cardiac repair after transplantation into infarcted hearts compared to myoblasts, which we partially attributed to MDSC's higher antioxidant levels.

aimTo determine if antioxidant treatment could increase myoblast survival, subsequently improving cardiac function after myoblast transplantation into infarcted hearts. MATERIALS AND

methodsMyoblasts were pre-treated with the antioxidant N-acetylcysteine (NAC) or the glutathione depleter, diethyl maleate (DEM), and injected into infarcted murine hearts. Regenerative potential was monitored by cell survival and cardiac function.

resultsAt early time points, hearts injected with NAC-treated myoblasts exhibited increased donor cell survival, greater cell proliferation, and decreased cellular apoptosis, compared to untreated myoblasts. NAC-treated myoblasts significantly improved cardiac contractility, reduced fibrosis, and increased vascular density compared to DEM-treated myoblasts, but compared to untreated myoblasts, no difference was noted. DISCUSSION: While early survival of myoblasts transplanted into infarcted hearts was augmented by NAC pre-treatment, cardiac function remained unchanged compared to non-treated myoblasts.

conclusionDespite improving cell survival with NAC treated myoblast transplantation in a MI heart, cardiac function remained similar to untreated myoblasts. These results suggest that the reduced cardiac regenerative potential of myoblasts, when compared to MDSCs, is not only attributable to cell survival but is probably also related to the secretion of paracrine factors by the MDSCs.

Indexed as

antioxidantscardiac functionmyoblast transplantationmyocardial infarctionoxidative stress

Identifiers

PMID28989945
PMCPMC5627517
OpenAlexW3022314355

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Registered trials

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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.