Evidence map›Paper›PMID 25007874›Full record

ArticleAmerican journal of physiology. Renal physiology2014

Pharmacological and genetic depletion of fibrinogen protects from kidney fibrosis.

Florin L Craciun, Amrendra K Ajay, Dana Hoffmann, Janani Saikumar, Steven L Fabian, Vanesa Bijol, Benjamin D Humphreys, Vishal S Vaidya

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Renal physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

36 citing papers in PubMed, 63 citations in OpenAlex.

  1. Review
  2. Nicotinamide Attenuates Complement and Coagulation Pathways and Resultant Renal Fibrosis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
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  13. TubularInternational journal of molecular sciences · 2022
    Article
  14. Article
  15. Article
  16. Folic acid-induced animal model of kidney disease.Animal models and experimental medicine · 2021
    Review
  17. Article
  18. Article
  19. Article
  20. Article
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

8 authors at 1 institution in 1 country.

Florin L CraciunDepartment of Medicine, Renal Division, Brigham and Women's Hospital, Boston, Massachusetts;
Amrendra K AjayDepartment of Medicine, Renal Division, Brigham and Women's Hospital, Boston, Massachusetts;
Dana HoffmannDepartment of Medicine, Renal Division, Brigham and Women's Hospital, Boston, Massachusetts;
Janani SaikumarDepartment of Medicine, Renal Division, Brigham and Women's Hospital, Boston, Massachusetts;
Steven L FabianDepartment of Medicine, Renal Division, Brigham and Women's Hospital, Boston, Massachusetts;
Vanesa BijolDepartment of Pathology, Brigham and Women's Hospital, Boston, Massachusetts;
Benjamin D HumphreysDepartment of Medicine, Renal Division, Brigham and Women's Hospital, Boston, Massachusetts;
Vishal S VaidyaDepartment of Medicine, Renal Division, Brigham and Women's Hospital, Boston, Massachusetts; Department of Environmental Health, Harvard School of Public Health, Boston, Massachusetts; and Harvard Program in Therapeutic Sciences, Harvard Medical School, Boston, Massachusetts vvaidya@partners.org.
Brigham and Women's Hospital · US

Funding

Role of SMOC2 in Kidney FibrosisR01ES017543 · NIEHS · BRIGHAM AND WOMEN'S HOSPITAL · PI VAIDYA, VISHAL S. · 2011 to 2021
$3.9M
Role of SMOC2 in Kidney FibrosisR56ES017543 · NIEHS · BRIGHAM AND WOMEN'S HOSPITAL · PI VAIDYA, VISHAL S. · 2016 to 2016
$213k
NIEHS NIH HHS ES-017543NIEHS NIH HHS R01 ES017543NIEHS NIH HHS R56 ES017543
6 · The paper itself

Abstract

Fibrinogen (Fg) has been implicated in the pathogenesis of several fibrotic disorders by acting as a profibrotic ligand for a variety of cellular surface receptors and by modulating the provisional fibrin matrix formed after injury. We demonstrated increased renal Fg expression after unilateral ureteral obstruction and folic acid (FA) nephropathy in mice, respectively. Urinary Fg excretion was also increased in FA nephropathy. Using in vitro and in vivo approaches, our results suggested that IL-6 mediates STAT3 activation in kidney fibrosis and that phosphorylated (p)STAT3 binds to Fgα, Fgβ, and Fgγ promoters in the kidney to regulate their transcription. Genetically modified Fg heterozygous mice (∼75% of normal plasma Fg levels) exhibited only 3% kidney interstitial fibrosis and tubular atrophy after FA nephropathy compared with 24% for wild-type mice. Fibrinogenolysis through Ancrod administration after FA reduced interstitial fibrosis more than threefold compared with vehicle-treated control mice. Mechanistically, we show that Fg acts synergistically with transforming growth factor (TGF)-β1 to induce fibroblast proliferation and activates TGF-β1/pSMAD2 signaling. This study offers increased understanding of Fg expression and molecular interactions with TGF-β1 in the progression to kidney fibrosis and, importantly, indicates that fibrinogenolytics like Ancrod present a treatment opportunity for a yet intractable disease.

Indexed as

AncrodAnimalsDisease ProgressionFibrinogenFibrosisHep G2 CellsHumansInterleukin-6KidneyKidney DiseasesMaleMiceMice, Inbred BALB CMice, Inbred C57BLSmad2 ProteinSTAT3 Transcription FactorAncrodFibrinogenInterleukin-6Smad2 ProteinSmad2 protein, mouseStat3 protein, mouseSTAT3 Transcription FactorTransforming Growth Factor beta1Ancrodchronic kidney diseasefibrinogenkidney fibrosistransforming growth factor-β1

Identifiers

PMID25007874
PMCPMC4137131
OpenAlexW2105369234

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.