Evidence map›Paper›PMID 22435995›Full record

ArticleJournal of cellular and molecular medicine2012

Elastin overexpression by cell-based gene therapy preserves matrix and prevents cardiac dilation.

Shu-Hong Li, Zhuo Sun, Lily Guo, Mihan Han, Michael F G Wood, Nirmalya Ghosh, I Alex Vitkin, Richard D Weisel, Ren-Ke Li

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
4.7field-weighted citation impact, top 5% 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

20 citing papers in PubMed, 39 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Role of elastic fiber degradation in disease pathogenesis.Biochimica et biophysica acta. Molecular basis of disease · 2023
    Review
  5. Article
  6. Article
  7. Review
  8. Dual-ContrastCirculation. Cardiovascular imaging · 2018
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Biomechanics of Cardiac Function.Comprehensive Physiology · 2015
    Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
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

9 authors at 1 institution in 1 country.

Shu-Hong LiDivision of Cardiovascular Surgery and Toronto General Research Institute, University Health Network, University of Toronto, Toronto, ON, Canada.
Zhuo Sun
Lily Guo
Mihan Han
Michael F G Wood
Nirmalya Ghosh
I Alex Vitkin
Richard D Weisel
Ren-Ke Li
University Health Network · CA

Funding

Canadian Institutes of Health Research MOP102535
6 · The paper itself

Abstract

After a myocardial infarction, thinning and expansion of the fibrotic scar contribute to progressive heart failure. The loss of elastin is a major contributor to adverse extracellular matrix remodelling of the infarcted heart, and restoration of the elastic properties of the infarct region can prevent ventricular dysfunction. We implanted cells genetically modified to overexpress elastin to re-establish the elastic properties of the infarcted myocardium and prevent cardiac failure. A full-length human elastin cDNA was cloned, subcloned into an adenoviral vector and then transduced into rat bone marrow stromal cells (BMSCs). In vitro studies showed that BMSCs expressed the elastin protein, which was deposited into the extracellular matrix. Transduced BMSCs were injected into the infarcted myocardium of adult rats. Control groups received either BMSCs transduced with the green fluorescent protein gene or medium alone. Elastin deposition in the infarcted myocardium was associated with preservation of myocardial tissue structural integrity (by birefringence of polarized light; P < 0.05 versus controls). As a result, infarct scar thickness and diastolic compliance were maintained and infarct expansion was prevented (P < 0.05 versus controls). Over a 9-week period, rats implanted with BMSCs demonstrated better cardiac function than medium controls; however, rats receiving BMSCs overexpressing elastin showed the greatest functional improvement (P < 0.01). Overexpression of elastin in the infarcted heart preserved the elastic structure of the extracellular matrix, which, in turn, preserved diastolic function, prevented ventricular dilation and preserved cardiac function. This cell-based gene therapy provides a new approach to cardiac regeneration.

Indexed as

AdenoviridaeAnimalsCardiomegalyCicatrixCloning, MolecularDiastoleElastinExtracellular MatrixFemaleGenetic TherapyGenetic VectorsHeartHeart FailureMesenchymal Stem CellsMyocardial InfarctionOrganisms, Genetically ModifiedElastin

Identifiers

PMID22435995
PMCPMC3823437
OpenAlexW1973816835

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.