Evidence map›Paper›PMID 23800850›Full record

ArticlePhysiological genomics2013

A novel genetic locus modulates infarct volume independently of the extent of collateral circulation.

Pei-Lun Chu, Sehoon Keum, Douglas A Marchuk

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 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

21 citing papers in PubMed, 30 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. The impact of native leptomeningeal collateralization on rapid blood flow recruitment following ischemic stroke.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2020
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Robust effects of genetic background on responses to subarachnoid hemorrhage in mice.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2016
    Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Review
  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

3 authors at 1 institution in 1 country.

Pei-Lun ChuUniversity Program in Genetics and Genomics and the Department of Molecular Genetics and Microbiology, Duke University School of Medicine, Durham, NC 27710, USA.
Sehoon Keum
Douglas A Marchuk
Duke University · US

Funding

Kidney Disease and InflammationT32DK072922 · NIDDK · UNIVERSITY OF VIRGINIA · PI OKUSA, MARK DOUGLAS · 2006 to 2020
$2.6M
Natural genetic variation regulating infarct volumeR01HL097281 · NHLBI · DUKE UNIVERSITY · PI MARCHUK, DOUGLAS A. · 2009 to 2012
$1.6M
NHLBI NIH HHS 1R01 HL-097281NHLBI NIH HHS R01 HL097281NIDDK NIH HHS T32 DK072922
6 · The paper itself

Abstract

In the mouse model of permanent, middle cerebral artery occlusion, infarct volume varies widely across inbred strains but generally is inversely correlated with collateral vessel number. However, we also observed certain mouse strains that share similar collateral vessel anatomy but exhibit significantly different infarct volume. To identify genetic factors determining infarct volume in a collateral vessel-independent manner, we performed quantitative trait locus analysis on a F2 cross between C57BL/6J and C3H/HeJ strains. We mapped four novel loci (Civq4 through Civq7) that modulate infarct volume. Civq4, on chromosome 8, is the strongest locus (logarithm of the odds 9.8) that contributes 21% of the phenotypic variance of infarct volume in the cross. The Civq4 and Civq6 loci represent transgressive B6 alleles that render animals susceptible to larger infarcts. Based on genomic sequence and microarray analyses, we propose candidate genes for the Civq4 locus. By selecting inbred strains with similar collateral vessel anatomy but that vary significantly in infarct volume, we have mapped four loci determining infarct volume in a mouse model of ischemic stroke. Two of the loci appear to modulate infarct volume through a collateral vessel-independent mechanism. Based on strain-specific sequence variants and differences in transcript levels, Msr1 and Mtmr7 appear to be strong candidate genes for Civq4. Identifying the underlying genetic factors of these loci will elucidate the genetic architecture response to cerebral ischemia, shed new light on disease mechanisms of ischemic stroke, and identify potential therapeutic targets for clinical applications.

Indexed as

Quantitative Trait LociAnimalsBrain InfarctionBrain IschemiaChromosome MappingCollateral CirculationDisease Models, AnimalGenetic LinkageMiceMice, Inbred C3HMice, Inbred C57BLPolymorphism, Single NucleotideProtein Tyrosine Phosphatases, Non-ReceptorScavenger Receptors, Class AMsr1 protein, mouseMtmr7 protein, mouseProtein Tyrosine Phosphatases, Non-ReceptorScavenger Receptors, Class Acollateral circulationischemic strokequantitative trait locusstroke geneticstransgressive segregation

Identifiers

PMID23800850
PMCPMC3763066
OpenAlexW2063961516

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.