Evidence map›Paper›PMID 20443117›Full record

ArticleMammalian genome : official journal of the International Mammalian Genome Society2010

Mitochondrial polymorphisms in rat genetic models of hypertension.

Sivarajan Kumarasamy, Kathirvel Gopalakrishnan, Asher Shafton, Jeremy Nixon, Jayakumar Thangavel, Phyllis Farms, Bina Joe

Open access · hybridAbstract read
In one paragraph

Article in Mammalian genome : official journal of the International Mammalian Genome Society, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.0field-weighted citation impact, top 24% 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

13 citing papers in PubMed, 17 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Mitochondrial DNA mutations and cardiovascular disease.Current opinion in cardiology · 2017
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Primarily screening and analyzing ESTs differentially expressed in rats' primary liver cancer.Chinese journal of cancer research = Chung-kuo yen cheng yen chiu · 2013
    Article
  12. Construction of two novel reciprocal conplastic rat strains and characterization of cardiac mitochondria.American journal of physiology. Heart and circulatory physiology · 2013
    Article
  13. 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

7 authors at 1 institution in 1 country.

Sivarajan KumarasamyPhysiological Genomics Laboratory, Department of Physiology and Pharmacology, University of Toledo College of Medicine, 3000 Arlington Avenue, Toledo, OH 43614-5804, USA.
Kathirvel Gopalakrishnan
Asher Shafton
Jeremy Nixon
Jayakumar Thangavel
Phyllis Farms
Bina Joe
University of Toledo · US

Funding

Genetics of HypertensionR01HL020176 · NHLBI · UNIVERSITY OF TOLEDO HEALTH SCI CAMPUS · PI JOE, BINA · 1985 to 2017
$8.1M
BIOCHEMISTRY AND GENETICS OF HYPERTENSIONR37HL020176 · NHLBI · UNIVERSITY OF TOLEDO HEALTH SCI CAMPUS · PI RAPP, JOHN P · 1993 to 2002
$1.6M
NHLBI NIH HHS HL020176NHLBI NIH HHS HL706709NHLBI NIH HHS R01 HL020176NHLBI NIH HHS R37 HL020176
6 · The paper itself

Abstract

Hypertension is a complex trait that has been studied extensively for genetic contributions of the nuclear genome. We examined mitochondrial genomes of the hypertensive strains: the Dahl Salt-Sensitive (S) rat, the Spontaneously Hypertensive Rat (SHR), and the Albino Surgery (AS) rat, and the relatively normotensive strains: the Dahl Salt-Resistant (R) rat, the Milan Normotensive Strain (MNS), and the Lewis rat (LEW). These strains were used previously for linkage analysis for blood pressure (BP) in our laboratory. The results provide evidence to suggest that variations in the mitochondrial genome do not account for observed differences in blood pressure between the S and R rats. However, variants were detected among the mitochondrial genomes of the various hypertensive strains, S, SHR, and AS, and also among the normotensive strains R, MNS, and LEW. A total of 115, 114, 106, 106, and 16 variations in mtDNA were observed between the comparisons S versus LEW, S versus MNS, S versus SHR, S versus AS, and SHR versus AS, respectively. Among the 13 genes coding for proteins of the electron transport chain, 8 genes had nonsynonymous variations between S, LEW, MNS, SHR, and AS. The lack of any sequence variants between the mitochondrial genomes of S and R rats provides conclusive evidence that divergence in blood pressure between these two inbred strains is exclusively programmed through their nuclear genomes. The variations detected among the various hypertensive strains provides the basis to construct conplastic strains and further evaluate the effects of these variants on hypertension and associated phenotypes.

Indexed as

Genes, MitochondrialPolymorphism, GeneticAnimalsGenetic LinkageHypertensionMitochondriaModels, AnimalPhenotypeRatsRats, Inbred DahlRats, Inbred SHRRats, Inbred Strains

Identifiers

PMID20443117
PMCPMC2890981
OpenAlexW2055361528

What OpenQuestion holds

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LicenceCC BY-NC
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Registered trials

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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.