Evidence map›Paper›PMID 16955284›Full record

ArticleNaunyn-Schmiedeberg's archives of pharmacology2006

Protection against myocardial ischemia/reperfusion injury by short-term diabetes: enhancement of VEGF formation, capillary density, and activation of cell survival signaling.

Guochuan Ma, Mohamed Al-Shabrawey, John A Johnson, Rahul Datar, Huda E Tawfik, Dehuang Guo, Ruth B Caldwell, R William Caldwell

Abstract read
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In one paragraph

Article in Naunyn-Schmiedeberg's archives of pharmacology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.1field-weighted citation impact, top 15% 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

33 citing papers in PubMed, 68 citations in OpenAlex.

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  19. Stress hyperglycemia: an essential survival response!Critical care (London, England) · 2013
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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 1 institution in 1 country.

Guochuan MaDepartment of Pharmacology & Toxicology, Medical College of Georgia, Augusta, GA, 30912, USA.
Mohamed Al-Shabrawey
John A Johnson
Rahul Datar
Huda E Tawfik
Dehuang Guo
Ruth B Caldwell
R William Caldwell
Augusta University · US

Funding

BLOOD/RETINAL BARRIER CHANGES IN RETINOPATHYR01EY004618 · NEI · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI CALDWELL, RUTH B · 1985 to 2010
$3.0M
L-arginine metabolism in diabetes-induced coronary dysfunctionR01HL070215 · NHLBI · MEDICAL COLLEGE OF GEORGIA (MCG) · PI CALDWELL, ROBERT WILLIAM · 2002 to 2011
$2.3M
NEI NIH HHS EY04618NHLBI NIH HHS HL70215
6 · The paper itself

Abstract

The aims of this study were to determine effects of diabetes duration on myocardial ischemia/reperfusion (I/R) injury and test whether time-dependent differences in sensitivity of the streptozotocin diabetic rat heart to I/R are related to differences in vascular density, levels of vascular endothelial growth factor (VEGF) or endothelial nitric oxide synthase (eNOS) expression, NO formation, activation of Akt, and/or oxidative stress. After 2 or 6 weeks of streptozotocin-induced diabetes, I/R injury was induced by occlusion (30 min) and reperfusion of the left descending coronary artery. After 2 weeks of diabetes, infarct size and cleavage of caspase-3, a proapoptosis signal, were decreased as compared with normoglycemic controls or rats that had been diabetic for 6 weeks, whereas capillary density and levels of VEGF and eNOS protein and cardiac NO(x) levels were all increased. Phosphorylation of Akt, a prosurvival signal, was also significantly increased after 2 weeks of diabetes. Cardiac lipid peroxidation was comparable to controls after 2 weeks of diabetes, whereas levels of nitrotyrosine, a peroxynitrite biomarker, were reduced. After 6 weeks of diabetes, lipid peroxidation was increased and levels of VEGF and plasma NO were reduced as compared with controls or rats diabetic for 2 weeks. Our results indicate endogenous cardioprotective mechanisms become transiently activated in this early stage of diabetes and that this may protect the heart from I/R injury through enhancement of VEGF and eNOS expression, NO formation, activation of cell survival signals, and decreased oxidative stress.

Indexed as

AnimalsBlood PressureBlotting, WesternCapillariesCaspase 3Cell SurvivalCoronary CirculationDiabetes Mellitus, ExperimentalHeart RateLipid PeroxidationMaleMyocardial Reperfusion InjuryMyocardiumNeovascularization, PhysiologicNitric OxideNitric Oxide Synthase Type III3-nitrotyrosineCaspase 3Nitric OxideNitric Oxide Synthase Type IIIOncogene Protein v-aktTyrosineVascular Endothelial Growth Factor A

Identifiers

PMID16955284
OpenAlexW2012410120

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.