Evidence map›Paper›PMID 18449560›Full record

ArticleHistochemistry and cell biology2008

Origin of renal myofibroblasts in the model of unilateral ureter obstruction in the rat.

Nicolas Picard, Oliver Baum, Alexander Vogetseder, Brigitte Kaissling, Michel Le Hir

Open access · hybridAbstract read
In one paragraph

Article in Histochemistry and cell biology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers.

0numbers the graph read from it
0cells of the map it votes in
80citing papers in PubMed
13.9field-weighted citation impact, top 1% 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

80 citing papers in PubMed, 146 citations in OpenAlex.

  1. Article
  2. Nanoparticles in the Treatment of Renal Fibrosis.International journal of nanomedicine · 2026
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  15. Article
  16. CaBritish journal of pharmacology · 2020
    Review
  17. Article
  18. Niao Du Kang Mixture Increases the Expression of mir-129-5p to Relieve Renal Fibrosis.Evidence-based complementary and alternative medicine : eCAM · 2020
    Article
  19. TGF-β1-p53 cooperativity regulates a profibrotic genomic program in the kidney: molecular mechanisms and clinical implications.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019
    Review
  20. Article

20 more citing papers are in PubMed but not listed here.

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

5 authors at 1 institution in 1 country.

Nicolas PicardAnatomical Institute, University of Zürich, Winterthurestr. 190, 8057, Zurich, Switzerland.
Oliver Baum
Alexander Vogetseder
Brigitte Kaissling
Michel Le Hir
University of Zurich · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tubulo-interstitial fibrosis is a constant feature of chronic renal failure and it is suspected to contribute importantly to the deterioration of renal function. In the fibrotic kidney there exists, besides normal fibroblasts, a large population of myofibroblasts, which are supposedly responsible for the increased production of intercellular matrix. It has been proposed that myofibroblasts in chronic renal failure originate from the transformation of tubular cells via epithelial-mesenchymal transition (EMT) or from infiltration by bone marrow-derived precursors. Little attention has been paid to the possibility of a transformation of resident fibroblasts into myofibroblasts in renal fibrosis. Therefore we examined the fate of resident fibroblasts in the initial phase of renal fibrosis in the classical model of unilateral ureter obstruction (UUO) in the rat. Rats were perfusion-fixed on days 1, 2, 3 and 4 after ligature of the right ureter. Starting from 1 day of UUO an increasing expression of alpha-smooth muscle actin (alphaSMA) in resident fibroblasts was revealed by immunofluorescence and confirmed by the observation of bundles of microfilaments and webs of intermediate filaments in the electron microscope. Inversely, there was a decreased expression of 5'-nucleotidase (5'NT), a marker of renal cortical fibroblasts. The RER became more voluminous, suggesting an increased synthesis of matrix. Intercellular junctions, a characteristic feature of myofibroblasts, became more frequent. The mitotic activity in fibroblasts was strongly increased. Renal tubules underwent severe regressive changes but the cells retained their epithelial characteristics and there was no sign of EMT. In conclusion, after ureter ligature, resident peritubular fibroblasts proliferated and they showed progressive alterations, suggesting a transformation in myofibroblasts. Thus the resident fibroblasts likely play a central role in fibrosis in that model.

Indexed as

ActinsAnimalsCalcium-Binding ProteinsCollagen Type IDisease Models, AnimalExtracellular MatrixFibroblastsFibrosisKidneyMaleMicroscopy, Electron, TransmissionMyoblastsRatsRats, Sprague-DawleyS100 Calcium-Binding Protein A4S100 ProteinsActinsCalcium-Binding ProteinsCollagen Type IS100a4 protein, ratS100 Calcium-Binding Protein A4S100 Proteins

Identifiers

PMID18449560
PMCPMC2413112
OpenAlexW2124572189

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.