Evidence map›Paper›PMID 20576932›Full record

ArticleCirculation research2010

Genetic architecture underlying variation in extent and remodeling of the collateral circulation.

Shiliang Wang, Hua Zhang, Xuming Dai, Robert Sealock, James E Faber

Abstract readComparative Study
In one paragraph

Article in Circulation research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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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

56 citing papers in PubMed.

  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
    Review
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  8. Review
  9. 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
    Article
  10. Cortical spreading depolarization-induced constriction of penetrating arteries can cause watershed ischemia: A potential mechanism for white matter lesions.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2023
    Article
  11. Review
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  14. Hypoxia induces de novo formation of cerebral collaterals and lessens the severity of ischemic stroke.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2020
    Article
  15. Article
  16. An exploratory investigation of brain collateral circulation plasticity after cerebral ischemia in two experimental C57BL/6 mouse models.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2020
    Article
  17. Article
  18. Review
  19. Article
  20. Strain-Dependent Variation in Acute Ischemic Muscle Injury.The American journal of pathology · 2018
    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.

Shiliang WangDepartment of Cell and Molecular Physiology and the McAllister Heart Institute, University of North Carolina at Chapel Hill, NC 27599-7545, USA.
Hua Zhang
Xuming Dai
Robert Sealock
James E Faber

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
UNC-Clinician-Scientist Training Program in Cardiovascular MedicineT32HL083828 · NHLBI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI STOUFFER, GEORGE A · 2006 to 2015
$2.0M
NHLBI NIH HHS HL090655NHLBI NIH HHS HL62584NHLBI NIH HHS R01 HL062584NHLBI NIH HHS R01 HL090655NHLBI NIH HHS T32 HL083828
6 · The paper itself

Abstract

rationaleCollaterals are arteriole-to-arteriole anastomoses that connect adjacent arterial trees. They lessen ischemic tissue injury by serving as endogenous bypass vessels when the trunk of 1 tree becomes narrowed by vascular disease. The number and diameter ("extent") of native (preexisting) collaterals, plus their amount of lumen enlargement (growth/remodeling) in occlusive disease, show remarkably wide variation among inbred mouse strains (eg, C57BL/6 and BALB/c), resulting in large differences in tissue injury in models of occlusive disease. Evidence suggests similar large differences exist among healthy humans.

objectiveTo identify candidate loci responsible for genetic-dependent collateral variation. METHODS AND

resultsCerebral collateral number and diameter were determined in 221 C57BL/6xBALB/c F2 progeny, followed by linkage analysis to identify quantitative trait loci (QTL) for collateral number and diameter. Four QTL were obtained for collateral number, including epistasis between 2 loci. A QTL that was identical to the strongest QTL for collateral number on chromosome 7 (logarithm of the odds [LOD]=29, effect size=37%) was also mapped for collateral diameter (LOD=17, effect size=30%). Chromosome substitution strain analysis confirmed this locus. We also obtained a unique QTL on chromosome 11 for collateral remodeling after middle cerebral artery occlusion. Association mapping within the chromosome 7 QTL interval using collateral traits measured for 15 inbred strains delineated 172-kbp (P=0.00002) and 290-kbp (P=0.0004) regions on chromosome 7 containing 2 and 7 candidate genes, respectively.

conclusionsWe conclude that collateral extent and remodeling are unique, highly heritable complex traits, with 1 QTL predominantly affecting native collateral number and diameter.

Indexed as

AnimalsBrainBrain MappingCollateral CirculationCrosses, GeneticGenetic LinkageGenetic VariationInfarction, Middle Cerebral ArteryMiceMice, Inbred AMice, Inbred BALB CMice, Inbred C57BLQuantitative Trait LociSpecies Specificity

Identifiers

PMID20576932
PMCPMC2924933

What OpenQuestion holds

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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.