Evidence map›Paper›PMID 22573106›Full record

ArticleAmerican journal of physiology. Regulatory, integrative and comparative physiology2012

Growth and regression of vasculature in healthy and diabetic mice after hindlimb ischemia.

Natalia Landázuri, Giji Joseph, Robert E Guldberg, W Robert Taylor

Abstract readComparative Study
In one paragraph

Article in American journal of physiology. Regulatory, integrative and comparative physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
–field-weighted citation impact
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

20 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
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  14. Review
  15. Article
  16. Tipping the balance from angiogenesis to fibrosis in CKD.Kidney international supplements · 2014
    Review
  17. Article
  18. Article
  19. Quantitative optical imaging of vascular response in vivo in a model of peripheral arterial disease.American journal of physiology. Heart and circulatory physiology · 2013
    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

4 authors.

Natalia LandázuriDivision of Cardiology, Department of Medicine, Emory University, Atlanta, GA, USA.
Giji Joseph
Robert E Guldberg
W Robert Taylor

Funding

T cell triggering events and hypertensionP01HL095070 · NHLBI · EMORY UNIVERSITY · PI JO, HANJOONG · 2009 to 2019
$20.5M
REGULATION OF OSTEOPONTIN EXPRESSION BY MECHANICAL STRAIR01HL062820 · NHLBI · EMORY UNIVERSITY · PI TAYLOR, WILLIAM ROBERT · 1999 to 2002
$927k
NHLBI NIH HHS P01 HL-095070NHLBI NIH HHS P01 HL095070NHLBI NIH HHS R01 HL062820NHLBI NIH HHS R01HL-062820
6 · The paper itself

Abstract

The formation of vascular networks during embryogenesis and early stages of development encompasses complex and tightly regulated growth of blood vessels, followed by maturation of some vessels, and spatially controlled disconnection and pruning of others. The adult vasculature, while more quiescent, is also capable of adapting to changing physiological conditions by remodeling blood vessels. Numerous studies have focused on understanding key factors that drive vessel growth in the adult in response to ischemic injury. However, little is known about the extent of vessel rarefaction and its potential contribution to the final outcome of vascular recovery. We addressed this topic by characterizing the endogenous phases of vascular repair in a mouse model of hindlimb ischemia. We showed that this process is biphasic. It encompasses an initial rapid phase of vessel growth, followed by a later phase of vessel rarefaction. In healthy mice, this process resulted in partial recovery of perfusion and completely restored the ability of mice to run voluntarily. Given that the ability to revascularize can be compromised by a cardiovascular risk factor such as diabetes, we also examined vascular repair in diabetic mice. We found that paradoxically both the initial growth and subsequent regression of collateral vessels were more pronounced in the setting of diabetes and resulted in impaired recovery of perfusion and impaired functional status. In conclusion, our findings demonstrate that the formation of functional collateral vessels in the hindlimb requires vessel growth and subsequent vessel rarefaction. In the setting of diabetes, the physiological defect was not in the initial formation of vessels but rather in the inability to sustain newly formed vessels.

Indexed as

AnimalsDiabetes Mellitus, ExperimentalDisease Models, AnimalHindlimbIschemiaLaser-Doppler FlowmetryMaleMiceMice, 129 StrainMice, Inbred C57BLNeovascularization, PhysiologicRegional Blood FlowStreptozocinStreptozocin

Identifiers

PMID22573106
PMCPMC3404641

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.