Evidence map›Paper›PMID 19834063›Full record

ArticleThe American journal of pathology2009

Effects of increased renal tubular vascular endothelial growth factor (VEGF) on fibrosis, cyst formation, and glomerular disease.

Samy Hakroush, Marcus J Moeller, Franziska Theilig, Brigitte Kaissling, Tjeerd P Sijmonsma, Manfred Jugold, Ann L Akeson, Milena Traykova-Brauch, Hiltraud Hosser, Brunhilde Hähnel and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed
6.7field-weighted citation impact, top 3% 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

62 citing papers in PubMed, 103 citations in OpenAlex.

  1. Review
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  9. Blocking CHOP-dependent TXNIP shuttling to mitochondria attenuates albuminuria and mitigates kidney injury in nephrotic syndrome.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
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  18. Article
  19. Evolving spectrum of diabetic nephropathy.World journal of diabetes · 2019
    Review
  20. Review

2 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

13 authors at 6 institutions in 4 countries.

Samy HakroushCentrum für Biomedizin und Medizintechnik Mannheim, University of Heidelberg, Germany.
Marcus J Moeller
Franziska Theilig
Brigitte Kaissling
Tjeerd P Sijmonsma
Manfred Jugold
Ann L Akeson
Milena Traykova-Brauch
Hiltraud Hosser
Brunhilde Hähnel
Hermann-Josef Gröne
Robert Koesters
Wilhelm Kriz
Heidelberg University · DEGerman Cancer Research Center · DECharité - Universitätsmedizin Berlin · DECincinnati Children's Hospital Medical Center · USUniversity of Zurich · CHWestfälische Hochschule · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The role of vascular endothelial growth factor (VEGF) in renal fibrosis, tubular cyst formation, and glomerular diseases is incompletely understood. We studied a new conditional transgenic mouse system [Pax8-rtTA/(tetO)(7)VEGF], which allows increased tubular VEGF production in adult mice. The following pathology was observed. The interstitial changes consisted of a ubiquitous proliferation of peritubular capillaries and fibroblasts, followed by deposition of matrix leading to a unique kind of fibrosis, ie, healthy tubules amid a capillary-rich dense fibrotic tissue. In tubular segments with high expression of VEGF, cysts developed that were surrounded by a dense network of peritubular capillaries. The glomerular effects consisted of a proliferative enlargement of glomerular capillaries, followed by mesangial proliferation. This resulted in enlarged glomeruli with loss of the characteristic lobular structure. Capillaries became randomly embedded into mesangial nodules, losing their filtration surface. Serum VEGF levels were increased, whereas endogenous VEGF production by podocytes was down-regulated. Taken together, this study shows that systemic VEGF interferes with the intraglomerular cross-talk between podocytes and the endocapillary compartment. It suppresses VEGF secretion by podocytes but cannot compensate for the deficit. VEGF from podocytes induces a directional effect, attracting the capillaries to the lobular surface, a relevant mechanism to optimize filtration surface. Systemic VEGF lacks this effect, leading to severe deterioration in glomerular architecture, similar to that seen in diabetic nephropathy.

Indexed as

CystsGlomerulonephritisKidney DiseasesKidney GlomerulusKidney TubulesAnimalsCapillariesFibrosisHumansIn Situ HybridizationMiceMice, TransgenicPodocytesVascular Endothelial Growth Factor AVascular Endothelial Growth Factor A

Identifiers

PMID19834063
PMCPMC2774053
OpenAlexW2145291136

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.