Evidence map›Paper›PMID 21044213›Full record

ReviewMicrocirculation (New York, N.Y. : 1994)2010

Spatial and temporal coordination of bone marrow-derived cell activity during arteriogenesis: regulation of the endogenous response and therapeutic implications.

Joshua K Meisner, Richard J Price

Open access · greenAbstract readReview
In one paragraph

Review in Microcirculation (New York, N.Y. : 1994), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

43 citing papers in PubMed, 52 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. MicroRNA-146a Regulates Perfusion Recovery in Response to Arterial OcclusionFrontiers in bioengineering and biotechnology · 2018
    Article
  12. Article
  13. Article
  14. Arteriogenesis in murine adipose tissue is contingent on CD68Microcirculation (New York, N.Y. : 1994) · 2017
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review
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

2 authors at 1 institution in 1 country.

Joshua K MeisnerDepartment of Biomedical Engineering, University of Virginia, Charlottesville, Virginia, USA.
Richard J Price
University of Virginia · US

Funding

MEDICAL SCIENTIST TRAINING PROGRAMT32GM007267 · NIGMS · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI GARCIA-BLANCO, MARIANO A. · 1985 to 2024
$13.4M
Arteriogenesis by Ultrasonic Microbubble DestructionR01HL074082 · NHLBI · UNIVERSITY OF VIRGINIA · PI PRICE, RICHARD J. · 2006 to 2010
$1.7M
Molecular Transducers Linking Shear Stress to Capillary Sprouting and StabilityR21HL098632 · NHLBI · UNIVERSITY OF VIRGINIA · PI PRICE, RICHARD J. · 2010 to 2011
$424k
American Heart Association-American Stroke Association 09PRE2060385NHLBI NIH HHS 5R01HL074082NHLBI NIH HHS R01 HL074082NHLBI NIH HHS R21 HL098632
6 · The paper itself

Abstract

Arterial occlusive disease is the leading cause of morbidity and mortality throughout the developed world, which creates a significant need for effective therapies to halt disease progression. Despite success of animal and small-scale human therapeutic arteriogenesis studies, this promising concept for treating arterial occlusive disease has yielded largely disappointing results in large-scale clinical trials. One reason for this lack of successful translation is that endogenous arteriogenesis is highly dependent on a poorly understood sequence of events and interactions between bone marrow derived cells (BMCs) and vascular cells, which makes designing effective therapies difficult. We contend that the process follows a complex, ordered sequence of events with multiple, specific BMC populations recruited at specific times and locations. Here, we present the evidence suggesting roles for multiple BMC populations-from neutrophils and mast cells to progenitor cells-and propose how and where these cell populations fit within the sequence of events during arteriogenesis. Disruptions in these various BMC populations can impair the arteriogenesis process in patterns that characterize specific patient populations. We propose that an improved understanding of how arteriogenesis functions as a system can reveal individual BMC populations and functions that can be targeted for overcoming particular impairments in collateral vessel development.

Indexed as

Neovascularization, PhysiologicAnimalsArterial Occlusive DiseasesBone Marrow CellsCollateral CirculationHematopoietic Stem CellsHumansInflammationLeukocytesModels, CardiovascularSignal TransductionSystems Biology

Identifiers

PMID21044213
PMCPMC2974339
OpenAlexW1901418464

What OpenQuestion holds

Textmetadata
LicenceTDM
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.