Evidence map›Paper›PMID 16341057›Full record

ArticleGene therapy2006

Ring-Sp1 decoy oligonucleotide effectively suppresses extracellular matrix gene expression and fibrosis of rat kidney induced by unilateral ureteral obstruction.

Y-M Chae, K-K Park, I-K Lee, J-K Kim, C-H Kim, Y-C Chang

Abstract read
PubMed Publisher
In one paragraph

Article in Gene therapy, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.4field-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

15 citing papers in PubMed, 34 citations in OpenAlex.

  1. Review
  2. Review
  3. Gene therapy and kidney diseases.Molecular therapy. Methods & clinical development · 2024
    Review
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Transcription factor decoy against stem cells master regulators, Nanog and Oct-4: a possible approach for differentiation therapy.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015
    Article
  12. Article
  13. Review
  14. Article
  15. Review
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 3 institutions in 1 country.

Y-M ChaeDepartment of Pathology, Catholic University of Daegu School of Medicine, Daegu, Korea.
K-K Park
I-K Lee
J-K Kim
C-H Kim
Y-C Chang
Catholic University of Daegu · KRDongguk University · KRKyungpook National University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tubulointerstitial fibrosis is the consequence of an injury characterized by the accumulation of excess collagen and other extracellular matrix components, resulting in the destruction of the normal kidney architecture and subsequent loss of function. A transcription factor Sp1, originally described as a ubiquitous transcription factor, is involved in the basal expression of extracellular matrix genes and may, therefore, be important in fibrotic processes. Here, we report on the design of a ring-Sp1 decoy oligonucleotide, containing the consensus Sp1 binding sequence in a single decoy molecule without an open end, to create a novel therapeutic strategy for fibrosis. The ring-Sp1 decoy oligonucleotide is highly resistant to degradation by nucleases or serum compared to the conventional phosphorothioated double-stranded Sp1 decoy oligonucleotide, and effectively suppressed the expression of transforming growth factor-beta1 and fibronectin, the binding of Sp1 to the promoter region of these genes, and proliferation in response to serum in normal rat kidney fibroblasts. Moreover, treatment with the ring-Sp1 decoy in vivo significantly attenuates extracellular matrix gene expression in the rat kidney in which a unilateral ureteral obstruction had been induced. These results suggest that the ring-Sp1 decoy oligonucleotide represents promising therapeutic alternative to the conventional treatment of fibrotic disorders.

Indexed as

AnimalsBlotting, NorthernCell LineCell ProliferationElectrophoretic Mobility Shift AssayExtracellular MatrixFibrosisGenetic EngineeringGenetic TherapyImmunohistochemistryKidneyMaleRatsRats, Sprague-DawleySp1 Transcription FactorTransfectionSp1 Transcription FactorTransforming Growth Factor beta

Identifiers

PMID16341057
OpenAlexW1995300918

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.