Evidence map›Paper›PMID 23249995›Full record

ArticlePhysiological genomics2013

Heterozygous knockout of transforming growth factor-β1 protects Dahl S rats against high salt-induced renal injury.

Chun Cheng Andy Chen, Aron M Geurts, Howard J Jacob, Fan Fan, Richard J Roman

Abstract read
In one paragraph

Article in Physiological genomics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.0field-weighted citation impact, top 25% 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

17 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Increased Levels of Renal Lysophosphatidic Acid in Rodent Models with Renal Disease.The Journal of pharmacology and experimental therapeutics · 2021
    Article
  6. Review
  7. Review
  8. Review
  9. Journal of the American Society of Nephrology : JASN · 2020
    Article
  10. Review
  11. Article
  12. Article
  13. Renal autoregulation in health and disease.Physiological reviews · 2015
    Review
  14. Article
  15. Article
  16. Review
  17. 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

5 authors at 2 institutions in 1 country.

Chun Cheng Andy ChenDepartment of Pharmacology and Toxicology, University of Mississippi Medical Center, Jackson, Mississippi 39211, USA.
Aron M Geurts
Howard J Jacob
Fan Fan
Richard J Roman
University of Mississippi Medical Center · USMedical College of Wisconsin · US

Funding

Mechanistic characterization of genes for hypertension and renal disease.RC2HL101681 · NHLBI · MEDICAL COLLEGE OF WISCONSIN · PI JACOB, HOWARD J · 2009 to 2010
$6.6M
20-HETE-TGF-beta in Hypertension-Induced Renal InjuryR37HL036279 · NHLBI · UNIVERSITY OF MISSISSIPPI MED CTR · PI ROMAN, RICHARD J. · 2005 to 2014
$4.0M
VASA RECTA HEMODYNAMICS IN GENETIC HYPERTENSIONR01HL036279 · NHLBI · MEDICAL COLLEGE OF WISCONSIN · PI ROMAN, RICHARD J. · 1986 to 2004
$1.3M
NHLBI NIH HHS HL-036279NHLBI NIH HHS HL-101681NHLBI NIH HHS R37 HL036279
6 · The paper itself

Abstract

The present study employed a zinc-finger nuclease strategy to create heterozygous knockout (KO) rats for the transforming growth factor-β1 (Tgfb1) gene on the Dahl SS/Jr genetic background (TGF-β1(+/-) Dahl S). Intercrossing TGF-β1(+/-) rats did not produce any homozygous KO rats (66.4% +/-, 33.6% +/+), indicating that the mutation is embryonic lethal. Six-week-old wild-type (WT) littermates and TGF-β1(+/-) Dahl S rats were fed a 0.4% (low salt, LS) or 8% NaCl (high salt, HS) diet for 5 wk. Renal cortical expression of TGF-β1, urinary TGF-β1 excretion, proteinuria, glomerular injury and tubulointerstitial fibrosis, and systolic blood pressure were similar in WT and TGF-β1(+/-) Dahl S rats maintained on the LS diet. The expression and urinary excretion of TGF-β1 increased to a greater extent in WT than in TGF-β1(+/-)Dahl S rats fed an HS diet for 1 wk. Systolic blood pressure rose by the same extent to 235 ± 2 mmHg in WT and 239 ± 4 mmHg in TGF-β1(+/-) Dahl S rats fed a HS diet for 5 wk. However, urinary protein excretion was significantly lower in TGF-β1(+/-) Dahl S than in the WT animals. The degree of glomerular injury and renal cortical and outer medullary fibrosis was markedly less in TGF-β1(+/-) than in WT rats. These findings suggest that the loss of one copy of the TGF-β1 gene blunts the increase in renal TGF-β1 protein expression and slows the progression of proteinuria, glomerulosclerosis, and renal interstitial fibrosis in Dahl S rats fed an HS diet independently of changes in blood pressure.

Indexed as

AnimalsBase SequenceFibrosisGene Expression RegulationGene Knockout TechniquesHypertensionIntracellular Signaling Peptides and ProteinsKidneyKidney DiseasesMembrane ProteinsMolecular Sequence DataProteinuriaRatsRats, Inbred DahlTransforming Growth Factor beta1Transforming Growth Factor beta2Intracellular Signaling Peptides and ProteinsMembrane ProteinsnephrinNPHS2 proteinTransforming Growth Factor beta1Transforming Growth Factor beta2Transforming Growth Factor beta3

Identifiers

PMID23249995
PMCPMC3568879
OpenAlexW2019562224

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.