Evidence map›Paper›PMID 11423936›Full record

ArticleGene therapy2001

Adenovirus-mediated transfer of type IV collagen alpha5 chain cDNA into swine kidney in vivo: deposition of the protein into the glomerular basement membrane.

P Heikkilä, A Tibell, T Morita, Y Chen, G Wu, Y Sado, Y Ninomiya, E Pettersson, K Tryggvason

Abstract read
PubMed Publisher
In one paragraph

Article in Gene therapy, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

22 citing papers in PubMed, 62 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Genotype-Based Molecular Mechanisms in Alport Syndrome.Journal of the American Society of Nephrology : JASN · 2025
    Review
  5. Review
  6. Review
  7. Review
  8. Article
  9. Review
  10. Novel Therapies for Alport Syndrome.Frontiers in medicine · 2022
    Review
  11. Improving Molecular Therapy in the Kidney.Molecular diagnosis & therapy · 2020
    Review
  12. Article
  13. Collagen IV diseases: A focus on the glomerular basement membrane in Alport syndrome.Matrix biology : journal of the International Society for Matrix Biology · 2017
    Review
  14. Glomerular pathology in Alport syndrome: a molecular perspective.Pediatric nephrology (Berlin, Germany) · 2012
    Review
  15. Article
  16. Irradiation prolongs survival of Alport mice.Journal of the American Society of Nephrology : JASN · 2008
    Article
  17. Understanding hereditary diseases using the dog and human as companion model systems.Mammalian genome : official journal of the International Mammalian Genome Society · 2007
    Review
  18. Gene therapy targeting kidney diseases: routes and vehicles.Clinical and experimental nephrology · 2006
    Review
  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 5 institutions in 3 countries.

P HeikkiläDivision of Matrix Biology, Department of Medical Biochemistry and Biophysics.
A Tibell
T Morita
Y Chen
G Wu
Y Sado
Y Ninomiya
E Pettersson
K Tryggvason
Karolinska Institutet · SEStatistics Sweden · SEMatrix Research (United States) · USOkayama University · JPShigei Medical Research Institute · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gene therapy of Alport syndrome (hereditary nephritis) aims at the transfer of a corrected type IV collagen alpha chain gene into renal glomerular cells responsible for production of the glomerular basement membrane (GBM). A GBM network composed of type IV collagen molecules is abnormal in Alport syndrome which leads progressively to kidney failure. The most common X-linked form of the disease is caused by mutations in the gene for the alpha5(IV) chain, the alpha5 chain of type IV collagen. Full-length human alpha5(IV) cDNA was expressed in HT1080 cells with an adenovirus vector, and the recombinant alpha5(IV) chain was shown to assemble into heterotrimers consisting of alpha3(IV) and alpha4(IV) chains, utilizing a FLAG epitope in the recombinant alpha5(IV) chain. The results indicate that correction of the molecular defect in Alport syndrome is possible. Previously, we had developed an organ perfusion method for effective in vivo gene transfer into glomerular cells. In vivo perfusion of pig kidneys with the recombinant adenovirus resulted in expression of the alpha5(IV) chain in kidney glomeruli as shown by in situ hybridization and its deposition into the GBM was shown by immunohistochemistry. The results strongly suggest future possibilities for gene therapy of Alport syndrome.

Indexed as

AdenoviridaeAnimalsBasement MembraneCell LineCollagenGenetic TherapyGenetic VectorsHumansKidney GlomerulusModels, AnimalNephritis, HereditaryPerfusionRNA, MessengerSwineCollagenRNA, Messenger

Identifiers

PMID11423936
OpenAlexW2003986149

What OpenQuestion holds

Textmetadata
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.