Evidence map›Paper›PMID 19350108›Full record

ReviewThrombosis and haemostasis2009

Serine proteases, inhibitors and receptors in renal fibrosis.

Allison A Eddy

Open access · greenAbstract readReview
In one paragraph

Review in Thrombosis and haemostasis, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

43 citing papers in PubMed, 75 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Observational
  14. Article
  15. Targeting Phospholipase D4 Attenuates Kidney Fibrosis.Journal of the American Society of Nephrology : JASN · 2017
    Article
  16. Review
  17. Review
  18. Article
  19. Article
  20. 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

1 author at 1 institution in 1 country.

Allison A EddyUniversity of Washington, Head, Division of Pediatric Nephrology, Seattle Children's Hospital and Research Institute, USA. allison.eddy@seattlechildrens.org
Seattle Children's Hospital · US

Funding

ROLE OF SCAVENGER RECEPTORS IN RENAL FIBROSISP50DK044757 · NIDDK · VANDERBILT UNIVERSITY · PI FOGO, AGNES B. · 1992 to 2011
$11.5M
MOLECULAR MECHANISMS IN RENAL INTERSTITIAL FIBROSISR01DK054500 · NIDDK · SEATTLE CHILDREN'S HOSPITAL · PI EDDY, ALLISON AUDREY · 1999 to 2008
$2.8M
MOLECULAR MECHANISMS OF HEPATITIS B VIRAL PATHOGENESIS AND PERSISTENCEZ01DK054500 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI LIANG, T. JAKE · 1997 to 2008
$927k
Intramural NIH HHS Z01 DK054500NIDDK NIH HHS DK44757NIDDK NIH HHS P50 DK044757NIDDK NIH HHS R01 DK054500
6 · The paper itself

Abstract

Chronic kidney disease (CKD) is estimated to affect one in eight adults. Their kidney function progressively deteriorates as inflammatory and fibrotic processes damage nephrons. New therapies to prevent renal functional decline must build on basic research studies that identify critical cellular and molecular mediators. Plasminogen activator inhibitor-1 (PAI-1), a potent fibrosis-promoting glycoprotein, is one promising candidate. Absent from normal kidneys, PAI-1 is frequently expressed in injured kidneys. Studies in genetically engineered mice have demonstrated its potency as a pro-fibrotic molecule. Somewhat surprising, its ability to inhibit serine protease activity does not appear to be its primary pro-fibrotic effect in CKD. Both tissue-type plasminogen activator and plasminogen deficiency significantly reduced renal fibrosis severity after ureteral obstruction, while genetic urokinase (uPA) deficiency had no effect. PAI-1 expression is associated with enhanced recruitment of key cellular effectors of renal fibrosis - interstitial macrophages and myofibroblasts. The ability of PAI-1 to promote cell migration involves interactions with the low-density lipoprotein receptor-associate protein-1 and also complex interactions with uPA bound to its receptor (uPAR) and several leukocyte and matrix integrins that associate with uPAR as co-receptors. uPAR is expressed by several cell types in damaged kidneys, and studies in uPAR-deficient mice have shown that its serves a protective role. uPAR mediates additional anti-fibrotic effects - it interacts with specific co-receptors to degrade PAI-1 and extracellular collagens, and soluble uPAR has leukocyte chemoattractant properties. Molecular pathways activated by serine proteases and their inhibitor, PAI-1, are promising targets for future anti-fibrotic therapeutic agents.

Indexed as

Signal TransductionAnimalsCell MovementChronic DiseaseFibrinolysinFibroblastsFibrosisHumansKidneyKidney DiseasesKininogensLow Density Lipoprotein Receptor-Related Protein-1MacrophagesMembrane GlycoproteinsNephritisPlasminogen Activator Inhibitor 1FibrinolysinKininogensLow Density Lipoprotein Receptor-Related Protein-1Membrane GlycoproteinsMrc2 protein, mousePlasminogen Activator Inhibitor 1Receptors, Cell SurfaceReceptors, Urokinase Plasminogen ActivatorSerine EndopeptidasesSerpinsTissue Plasminogen ActivatorUrokinase-Type Plasminogen ActivatorVitronectin

Identifiers

PMID19350108
PMCPMC3136815
OpenAlexW2061853640

What OpenQuestion holds

Textmetadata
LicenceTDM
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.