Evidence map›Paper›PMID 21070849›Full record

ArticleFree radical biology & medicine2011

Dipyridamole reverses peripheral ischemia and induces angiogenesis in the Db/Db diabetic mouse hind-limb model by decreasing oxidative stress.

Christopher B Pattillo, Shyamal C Bir, Billy G Branch, Eric Greber, Xinggui Shen, Sibile Pardue, Rakesh P Patel, Christopher G Kevil

Open access · greenAbstract read
In one paragraph

Article in Free radical biology & medicine, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
3.9field-weighted citation impact, top 7% 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

17 citing papers in PubMed, 28 citations in OpenAlex.

  1. Review
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  6. Role of thiosulfate in hydrogen sulfide-dependent redox signaling in endothelial cells.American journal of physiology. Heart and circulatory physiology · 2017
    Article
  7. Bilirubin exerts pro-angiogenic property through Akt-eNOS-dependent pathway.Hypertension research : official journal of the Japanese Society of Hypertension · 2015
    Article
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  12. Review
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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

8 authors at 2 institutions in 1 country.

Christopher B PattilloDepartment of Pathology, Louisiana State University Health Sciences Center-Shreveport, Shreveport, LA 71130, USA.
Shyamal C Bir
Billy G Branch
Eric Greber
Xinggui Shen
Sibile Pardue
Rakesh P Patel
Christopher G Kevil
Louisiana State University Health Sciences Center Shreveport · USUniversity of Alabama at Birmingham · US

Funding

ICAM-1 governs angiogenesis and endothelial redox statusR01HL080482 · NHLBI · LOUISIANA STATE UNIV HSC SHREVEPORT · PI KEVIL, CHRISTOPHER G · 2006 to 2010
$1.8M
GCL-M Regulation of AngiogenesisF32HL094021 · NHLBI · LOUISIANA STATE UNIV HSC SHREVEPORT · PI PATTILLO, CHRISTOPHER BRUCE · 2008 to 2010
$149k
NHLBI NIH HHS F32 HL094021NHLBI NIH HHS HL080482NHLBI NIH HHS HL094021NHLBI NIH HHS R01 HL080482
6 · The paper itself

Abstract

Dipyridamole anti-platelet therapy has previously been suggested to ameliorate chronic tissue ischemia in healthy animals. However, it is not known if dipyridamole therapy represents a viable approach to alleviating chronic peripheral tissue ischemia associated with type 2 diabetes. Here we examine the hypothesis that dipyridamole treatment restores reperfusion of chronic hind-limb ischemia in the murine B6.BKS-Lepr(db/db) diabetic model. Dipyridamole therapy quickly rectified ischemic hind-limb blood flow to near preligation levels within 3 days of the start of therapy. Restoration of ischemic tissue blood flow was associated with increased vascular density and endothelial cell proliferation observed only in ischemic limbs. Dipyridamole significantly increased total nitric oxide metabolite levels in tissue, which were not associated with changes in endothelial NO synthase expression or phosphorylation. Interestingly, dipyridamole therapy significantly decreased ischemic tissue superoxide and protein carbonyl levels, identifying a dominant antioxidant mechanistic response. Dipyridamole therapy also moderately reduced diabetic hyperglycemia and attenuated development of dyslipidemia over time. Together, these data reveal that dipyridamole therapy is an effective modality for the treatment of chronic tissue ischemia during diabetes and highlights the importance of dipyridamole antioxidant activity in restoring tissue NO bioavailability during diabetes.

Indexed as

Disease Models, AnimalNeovascularization, PhysiologicOxidative StressAnimalsDiabetes Mellitus, ExperimentalDipyridamoleHindlimbHypercholesterolemiaIschemiaMiceMice, Inbred C57BLNitric OxideNitric Oxide Synthase Type IIIPhosphorylationReceptors, LeptinSuperoxidesDipyridamoleNitric OxideNitric Oxide Synthase Type IIIReceptors, LeptinSuperoxidesVascular Endothelial Growth Factor AVasodilator Agents

Identifiers

PMID21070849
PMCPMC4413947
OpenAlexW2011871990

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.