Evidence map›Paper›PMID 17504948›Full record

ArticlePhysiological genomics2007

Dissection of a genetic locus influencing renal function in the rat and its concordance with kidney disease loci on human chromosome 1q21.

Michael R Garrett, William T Gunning, Tracy Radecki, Arti Richard

Abstract readComparative Study
In one paragraph

Article in Physiological genomics, 2007. 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
1.4field-weighted citation impact, top 17% 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, 20 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Will the real Dahl S rat please stand up?American journal of physiology. Renal physiology · 2019
    Article
  5. Article
  6. Genetic susceptibility and loss of Nr4a1 enhances macrophage-mediated renal injury in CKD.Journal of the American Society of Nephrology : JASN · 2014
    Article
  7. A mutation in the start codon of γ-crystallin D leads to nuclear cataracts in the Dahl SS/Jr-Ctr strain.Mammalian genome : official journal of the International Mammalian Genome Society · 2013
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Evaluation of metalloprotease inhibitors on hypertension and diabetic nephropathy.American journal of physiology. Renal physiology · 2011
    Article
  13. Heterogeneous stock rats: a new model to study the genetics of renal phenotypes.American journal of physiology. Renal physiology · 2010
    Article
  14. Article
  15. Review
  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

4 authors at 1 institution in 1 country.

Michael R GarrettDepartment of Physiology, Pharmacology, Metabolism and Cardiovascular Sciences, University of Toledo, Health Science Campus, Toledo, Ohio, USA. mgarrett@mcw.edu
William T Gunning
Tracy Radecki
Arti Richard
University of Toledo · US

Funding

Genetic Analysis of Renal Disease in SHR and Dahl S RatsR01HL066998 · NHLBI · UNIVERSITY OF TOLEDO HEALTH SCI CAMPUS · PI GARRETT, MICHAEL R · 2001 to 2003
$802k
NHLBI NIH HHS R01 HL066998NHLBI NIH HHS R01-HL-066998
6 · The paper itself

Abstract

Previously, we conducted a genome scan on a population derived from the Dahl salt-sensitive hypertensive (S) and the spontaneously hypertensive rat (SHR) using urinary albumin excretion (UAE) as our primary measure of renal function. We identified 10 quantitative trait loci (QTL) linked to several renal and/or cardiovascular traits. In particular, linkage and subsequent congenic strain analysis demonstrated that the loci on chromosome 2 had a large and significant effect on UAE compared with the S rat. The present work sought to characterize the chromosome 2 congenic strain [S.SHR] by conducting a time-course analysis (week 4-20), including evaluating additional renal parameters, histology, electron microscopy, and gene expression/ pathway analysis. Throughout the time course the congenic strain consistently maintained a threefold reduction in UAE compared with S rats and was supported by the histological findings of significantly reduced glomerular, tubular and interstitial changes. Gene expression/pathway analysis performed at week 4, 12, and 20 revealed that pathways involved in cellular assembly and organization, cellular movement, and immune response were controlled differently between the S and congenic. When all the data are considered, the chromosome 2 congenic appears to attenuate renal damage primarily through an altered fibrotic response. Recombinant progeny testing was employed to reduce the QTL to approximately 1.5 cM containing several interesting candidate genes. The concordance of this rat QTL with renal disease loci on human chromosome 1q21 demonstrate that elucidating the causative gene and mechanism of the rat QTL may be of particular importance for understanding kidney disease in humans.

Indexed as

Chromosome MappingChromosomes, Human, Pair 1Genetic LinkageQuantitative Trait LociAnimalsGene Expression ProfilingHumansKidneyKidney DiseasesRatsRats, Inbred DahlRats, Inbred SHRSignal Transduction

Identifiers

PMID17504948
PMCPMC3153419
OpenAlexW1989631878

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.