Evidence map›Paper›PMID 18575881›Full record

ReviewHistochemistry and cell biology2008

The renal cortical interstitium: morphological and functional aspects.

Brigitte Kaissling, Michel Le Hir

Open access · hybridAbstract readReview
In one paragraph

Review 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 87 papers.

0numbers the graph read from it
0cells of the map it votes in
87citing papers in PubMed
4.4field-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

87 citing papers in PubMed, 171 citations in OpenAlex.

  1. Article
  2. The kidney stroma in development and disease.Nature reviews. Nephrology · 2025
    Review
  3. Article
  4. Molecular and Cellular Mediators of Renal Fibrosis in Lupus Nephritis.International journal of molecular sciences · 2025
    Review
  5. Article
  6. Review
  7. Review
  8. Acute kidney injury in diabetes mellitus: Epidemiology, diagnostic, and therapeutic concepts.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2023
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. The Mechanism of CD8Biomolecules · 2021
    Review
  15. Review
  16. Article
  17. Cell Cycle Dysregulation and Renal Fibrosis.Frontiers in cell and developmental biology · 2021
    Review
  18. Review
  19. Article
  20. Article

27 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

2 authors at 1 institution in 1 country.

Brigitte KaisslingInstitute of Anatomy, Division Vegetative Anatomy, University of Zürich, Winterthurerstr. 190, 8057, Zurich, Switzerland. brigitte.kaissling@access.uzh.ch
Michel Le Hir
University of Zurich · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The renal interstitial compartment, situated between basement membranes of epithelia and vessels, contains two contiguous cellular networks. One network is formed by interstitial fibroblasts, the second one by dendritic cells. Both are in intimate contact with each other. Fibroblasts are interconnected by junctions and connected to basement membranes of vessels and tubules by focal adhesions. Fibroblasts constitute the "skeleton" of the kidney. In the renal cortex, fibroblasts produce erythropoietin and are distinguished from other interstitial cells by their prominent F-actin cytoskeleton, abundance of rough endoplasmic reticulum, and by ecto-5'-nucleotidase expression in their plasma membrane. The resident dendritic cells belong to the mononuclear phagocyte system and fulfil a sentinel function. They are characterized by their expression of MHC class II and CD11c. The central situation of fibroblasts suggests that signals from tubules, vessels, and inflammatory cells converge in fibroblasts and elicit an integrated response. Following tubular damage and inflammatory signals fibroblasts proliferate, change to the myofibroblast phenotype and increase their collagen production, potentially resulting in renal fibrosis. The acquisition of a profibrotic phenotype by fibroblasts in renal diseases is generally considered a main causal event in the progression of chronic renal failure. However, it might also be seen as a repair process.

Indexed as

5'-NucleotidaseActinsAnimalsDendritic CellsErythropoietinFibroblastsFibrosisHumansKidney CortexKidney Failure, ChronicMiceNephritis, Interstitial5'-NucleotidaseActinsErythropoietin

Identifiers

PMID18575881
PMCPMC2491705
OpenAlexW2074983969

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.