Evidence map›Paper›PMID 22412848›Full record

ArticlePloS one2012

Genetic dissection of the Canq1 locus governing variation in extent of the collateral circulation.

Shiliang Wang, Hua Zhang, Tim Wiltshire, Robert Sealock, James E Faber

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
2.2field-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

34 citing papers in PubMed, 57 citations in OpenAlex.

  1. Genetic determinants of insufficiency of the collateral circulation.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2026
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  5. Large differences in collateral blood vessel abundance among individuals arise from multiple genetic variants.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2023
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  10. High-altitude rodents have abundant collaterals that protect against tissue injury after cerebral, coronary and peripheral artery occlusion.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2021
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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 1 institution in 1 country.

Shiliang WangDepartment of Physiology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, United States of America.
Hua Zhang
Tim Wiltshire
Robert Sealock
James E Faber
University of North Carolina at Chapel Hill · US

Funding

ALPHA ADRENOCEPTORS IN VASCULAR WALL GROWTHR01HL062584 · NHLBI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI FABER, JAMES E · 1999 to 2011
$4.6M
Mechanisms of Collateral Development and Collateral Growth in IschemiaR01HL090655 · NHLBI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI FABER, JAMES E · 2008 to 2011
$2.0M
Maintenance and Rarefaction of the Native Collateral CirculationR01HL111070 · NHLBI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI FABER, JAMES E · 2012 to 2015
$1.9M
NHLBI NIH HHS HL062584NHLBI NIH HHS HL090655NHLBI NIH HHS R01 HL062584NHLBI NIH HHS R01 HL090655NHLBI NIH HHS R01 HL111070
6 · The paper itself

Abstract

backgroundNative (pre-existing) collaterals are arteriole-to-arteriole anastomoses that interconnect adjacent arterial trees and serve as endogenous bypass vessels that limit tissue injury in ischemic stroke, myocardial infarction, coronary and peripheral artery disease. Their extent (number and diameter) varies widely among mouse strains and healthy humans. We previously identified a major quantitative trait locus on chromosome 7 (Canq1, LOD = 29) responsible for 37% of the heritable variation in collateral extent between C57BL/6 and BALB/c mice. We sought to identify candidate genes in Canq1 responsible for collateral variation in the cerebral pial circulation, a tissue whose strain-dependent variation is shared by similar variation in other tissues. METHODS AND

findingsCollateral extent was intermediate in a recombinant inbred line that splits Canq1 between the C57BL/6 and BALB/c strains. Phenotyping and SNP-mapping of an expanded panel of twenty-one informative inbred strains narrowed the Canq1 locus, and genome-wide linkage analysis of a SWRxSJL-F2 cross confirmed its haplotype structure. Collateral extent, infarct volume after cerebral artery occlusion, bleeding time, and re-bleeding time did not differ in knockout mice for two vascular-related genes located in Canq1, IL4ra and Itgal. Transcript abundance of 6 out of 116 genes within the 95% confidence interval of Canq1 were differentially expressed >2-fold (p-value<0.05÷150) in the cortical pia mater from C57BL/6 and BALB/c embryos at E14.5, E16.5 and E18.5 time-points that span the period of collateral formation.

conclusionsThese findings refine the Canq1 locus and identify several genes as high-priority candidates important in specifying native collateral formation and its wide variation.

Indexed as

Quantitative Trait LociAnimalsChromosome MappingChromosomes, MammalianCluster AnalysisCollateral CirculationGene ExpressionGene Expression ProfilingGenome-Wide Association StudyHemostasisMaleMiceMice, Inbred BALB CMice, Inbred C57BLMice, KnockoutPolymorphism, Single Nucleotide

Identifiers

PMID22412848
PMCPMC3295810
OpenAlexW2006278464

What OpenQuestion holds

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LicenceCC BY
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.