Evidence map›Paper›PMID 11914261›Full record

ArticleCirculation2002

Nitric oxide mediates the antiapoptotic effect of insulin in myocardial ischemia-reperfusion: the roles of PI3-kinase, Akt, and endothelial nitric oxide synthase phosphorylation.

Feng Gao, Erhe Gao, Tian-Li Yue, Eliot H Ohlstein, Bernard L Lopez, Theodore A Christopher, Xin-Liang Ma

Registry-linked trialOpen access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Circulation, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04133922 (Effect of GLP-1 on Microvascular Insulin Responses in Type 1 Diabetes), which is not on this map. Cited by 119 papers.

0numbers the graph read from it
0cells of the map it votes in
119citing papers in PubMed
14.5field-weighted citation impact, top 1% 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.

NCT04133922 early_phase1withdrawnstarted 2019, after this paper: background citation

Effect of GLP-1 on Microvascular Insulin Responses in Type 1 Diabetes

Ran2019Enrolled0Registered outcomes5Posted comparisons0ConditionsInsulin Sensitivity/Resistance, Type 1 DiabetesArmsDextrose 20 % in Water, GLP-1, Insulin
Open the trial in the graph
3 · Its place in the literature

Who cites it

119 citing papers in PubMed, 469 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Article
  5. Review
  6. Exploring the Action Mechanism of the Active Ingredient of Quercetin inEvidence-based complementary and alternative medicine : eCAM · 2022
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59 more citing papers are in PubMed but not listed here.

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

7 authors at 1 institution in 1 country.

Feng GaoDepartment of Emergency Medicine, Thomas Jefferson University, Philadelphia, Pa, USA.
Erhe Gao
Tian-Li Yue
Eliot H Ohlstein
Bernard L Lopez
Theodore A Christopher
Xin-Liang Ma
Air Force Medical University · CN

Funding

Peroxynitrite in Cardiac Ischemia/Reperfusion InjuryR01HL063828 · NHLBI · THOMAS JEFFERSON UNIVERSITY · PI MA, XIN-LIANG · 2001 to 2010
$2.5M
NHLBI NIH HHS HL-63828
6 · The paper itself

Abstract

backgroundRecent evidence from cultured endothelial cell studies suggests that phosphorylation of endothelial nitric oxide synthase (eNOS) through the PI3-kinase-Akt pathway increases NO production. This study was designed to elucidate the signaling pathway involved in the antiapoptotic effect of insulin in vivo and to test the hypothesis that phosphorylation of eNOS by insulin may participate in the cardioprotective effect of insulin after myocardial ischemia and reperfusion. METHODS AND

resultsMale Sprague-Dawley rats were subjected to 30 minutes of myocardial ischemia and 4 hours of reperfusion. Rats were randomized to receive vehicle, insulin, insulin plus wortmannin, or insulin plus L-NAME. Treatment with insulin resulted in 2.6-fold and 4.3-fold increases in Akt and eNOS phosphorylation and a significant increase in NO production in ischemic/reperfused myocardial tissue. Phosphorylation of Akt and eNOS and increase of NO production by insulin were completely blocked by wortmannin, a PI3-kinase inhibitor. Pretreatment with L-NAME, a nonselective NOS inhibitor, had no effect on Akt and eNOS phosphorylation but significantly reduced NO production. Moreover, treatment with insulin markedly reduced myocardial apoptotic death (P<0.01 versus vehicle). Pretreatment with wortmannin abolished the antiapoptotic effect of insulin. Most importantly, pretreatment with L-NAME also significantly reduced the antiapoptotic effect of insulin (P<0.01 versus insulin).

conclusionsThese results demonstrated that in vivo administration of insulin activated Akt through the PI3-kinase-dependent mechanism and reduced postischemic myocardial apoptotic death. Phosphorylation of eNOS and the concurrent increase of NO production contribute significantly to the antiapoptotic effect of insulin.

Indexed as

ApoptosisProtein Serine-Threonine KinasesAndrostadienesAnimalsCells, CulturedEnzyme ActivationEnzyme InhibitorsGlucoseInsulinMaleMyocardial IschemiaMyocardiumNG-Nitroarginine Methyl EsterNitric OxideNitric Oxide SynthaseNitric Oxide Synthase Type IIIAkt1 protein, ratAndrostadienesEnzyme InhibitorsGlucoseInsulinNG-Nitroarginine Methyl EsterNitric OxideNitric Oxide SynthaseNitric Oxide Synthase Type IIINos3 protein, ratPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsPotassiumProtein Serine-Threonine KinasesProto-Oncogene ProteinsProto-Oncogene Proteins c-aktWortmannin

Identifiers

PMID11914261
OpenAlexW2022131685

What Socratic holds

Textmetadata
Read underepoch 390

Registered trials

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 Socratic graph.