Evidence map›Paper›PMID 11696434›Full record

ArticleThe American journal of pathology2001

The distribution and regulation of integrin-linked kinase in normal and diabetic kidneys.

L Guo, P W Sanders, A Woods, C Wu

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.1field-weighted citation impact, top 14% 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

24 citing papers in PubMed, 84 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. Review
  11. Article
  12. Article
  13. New insights into epithelial-mesenchymal transition in kidney fibrosis.Journal of the American Society of Nephrology : JASN · 2010
    Review
  14. Article
  15. Abnormalities in signaling pathways in diabetic nephropathy.Expert review of endocrinology & metabolism · 2010
    Article
  16. Inhibition of integrin-linked kinase attenuates renal interstitial fibrosis.Journal of the American Society of Nephrology : JASN · 2009
    Article
  17. Article
  18. Article
  19. Up-regulation of integrin-linked kinase in the streptozotocin-induced diabetic rat retina.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2007
    Article
  20. The parvins.Cellular and molecular life sciences : CMLS · 2006
    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

4 authors at 2 institutions in 1 country.

L GuoDepartment of Cell Biology and the Cell Adhesion and Matrix Research Center, University of Alabama at Birmingham, Birmingham, Alabama, USA.
P W Sanders
A Woods
C Wu
University of Alabama at Birmingham · USMatrix Research (United States) · US

Funding

The PINCH-ILK-parvin complexes in glomerular cellsR01DK054639 · NIDDK · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI WU, CHUANYUE · 1998 to 2010
$3.2M
Salt-Sensitive Hypertension/Hypertensive NephrosclerosisR01DK046199 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI SANDERS, PAUL W. · 1992 to 2011
$2.9M
NIDDK NIH HHS DK46199NIDDK NIH HHS DK54639NIDDK NIH HHS R01 DK046199NIDDK NIH HHS R01 DK054639
6 · The paper itself

Abstract

Alteration in cell adhesion and extracellular matrix deposition is a hallmark of diabetic glomerulosclerosis. Integrin-linked kinase (ILK) is a recently identified integrin cytoplasmic-binding protein that has been implicated in the regulation of cell adhesion and extracellular matrix deposition. To begin to investigate whether ILK is involved in the pathogenesis of diabetic glomerulosclerosis, we have analyzed the distribution and regulation of ILK in normal and diabetic kidneys as well as in isolated mesangial cells. We have found that ILK is normally expressed at high concentration in visceral epithelial cells. In diabetic glomeruli, ILK expression in the mesangium is dramatically increased. The increase in ILK level is associated with diffuse mesangial expansion. In glomeruli where advanced nodular sclerosis and global sclerosis were dominant, ILK level was reduced, suggesting that the increase in ILK expression likely associates with relatively early glomerulosclerosis. Additionally, we have found that exposure of mesangial cells to high concentrations of glucose significantly increased the ILK level. Finally, we show that ILK localizes to regions of cell membranes that are in close contact with mesangial fibronectin matrix. These results suggest that ILK is likely involved in mesangial matrix expansion in response to hyperglycemia in the pathogenesis of diabetic glomerulosclerosis.

Indexed as

AnimalsDiabetic NephropathiesExtracellular MatrixFibronectinsGlomerular MesangiumGlomerulosclerosis, Focal SegmentalHumansKidneyKidney GlomerulusProtein Serine-Threonine KinasesRatsReference ValuesScaffold Protein ILKTissue DistributionFibronectinsProtein Serine-Threonine KinasesScaffold Protein ILK

Identifiers

PMID11696434
PMCPMC1867072
OpenAlexW1994430096

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.