Evidence map›Paper›PMID 23349490›Full record

ArticleDiabetes2013

Enhanced NF-κB activity impairs vascular function through PARP-1-, SP-1-, and COX-2-dependent mechanisms in type 2 diabetes.

Modar Kassan, Soo-Kyoung Choi, Maria Galán, Alexander Bishop, Kazuo Umezawa, Mohamed Trebak, Souad Belmadani, Khalid Matrougui

Open access · bronzeAbstract read
In one paragraph

Article in Diabetes, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
2.6field-weighted citation impact, top 11% 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

54 citing papers in PubMed, 91 citations in OpenAlex.

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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 5 institutions in 2 countries.

Modar KassanDepartment of Physiology, Hypertension and Renal Center of Excellence, Tulane University, New Orleans, Louisiana, USA.
Soo-Kyoung Choi
Maria Galán
Alexander Bishop
Kazuo Umezawa
Mohamed Trebak
Souad Belmadani
Khalid Matrougui
Eastern Virginia Medical School · USTulane University · USAlbany Medical Center Hospital · USKeio University · JPThe University of Texas Health Science Center at San Antonio · US

Funding

Receptor-regulated Ca2+ Entry Pathways in Smooth MuscleR01HL097111 · NHLBI · STATE UNIVERSITY OF NEW YORK AT ALBANY · PI TREBAK, MOHAMED · 2010 to 2019
$3.7M
Mechanisms of Coronary Arteriolar Dysfunction in Type 2 DiabetesR01HL095566 · NHLBI · TULANE UNIVERSITY OF LOUISIANA · PI MATROUGUI, KHALID · 2010 to 2014
$1.8M
NHLBI NIH HHS 1R01HL095566NHLBI NIH HHS 5R01HL097111NHLBI NIH HHS R01 HL095566NHLBI NIH HHS R01 HL097111
6 · The paper itself

Abstract

Type 2 diabetes (T2D) is associated with vascular dysfunction. We hypothesized that increased nuclear factor-κB (NF-κB) signaling contributes to vascular dysfunction in T2D. We treated type 2 diabetic (db(-)/db(-)) and control (db(-)/db(+)) mice with two NF-κB inhibitors (6 mg/kg dehydroxymethylepoxyquinomicin twice a week and 500 μg/kg/day IKK-NBD peptide) for 4 weeks. Pressure-induced myogenic tone was significantly potentiated, while endothelium-dependent relaxation (EDR) was impaired in small coronary arterioles and mesenteric resistance artery from diabetic mice compared with controls. Interestingly, diabetic mice treated with NF-κB inhibitors had significantly reduced myogenic tone potentiation and improved EDR. Importantly, vascular function was also rescued in db(-)/db(-p50NF-κB-/-) and db(-)/db(-PARP-1-/-) double knockout mice compared with db(-)/db(-) mice. Additionally, the acute in vitro downregulation of NF-κB-p65 using p65NF-κB short hairpin RNA lentivirus in arteries from db(-)/db(-) mice also improved vascular function. The NF-κB inhibition did not affect blood glucose level or body weight. The RNA levels for Sp-1 and eNOS phosphorylation were decreased, while p65NF-κB phosphorylation, cleaved poly(ADP-ribose) polymerase (PARP)-1, and cyclooxygenase (COX)-2 expression were increased in arteries from diabetic mice, which were restored after NF-κB inhibition and in db(-)/db(-p50NF-κB-/-) and db(-)/db(-PARP-1-/-) mice. In the current study, we provided evidence that enhanced NF-κB activity impairs vascular function by PARP-1-, Sp-1-, and COX-2-dependent mechanisms in male type 2 diabetic mice. Therefore, NF-κB could be a potential target to overcome diabetes-induced vascular dysfunction.

Indexed as

AnimalsBenzamidesCells, CulturedCyclohexanonesCyclooxygenase 2Diabetes Mellitus, Type 2Endothelial CellsMaleMiceNF-kappa BPoly (ADP-Ribose) Polymerase-1Poly(ADP-ribose) PolymerasesReal-Time Polymerase Chain ReactionSp1 Transcription FactorBenzamidesCyclohexanonesCyclooxygenase 2dehydroxymethylepoxyquinomicinNF-kappa BParp1 protein, mousePoly (ADP-Ribose) Polymerase-1Poly(ADP-ribose) PolymerasesSp1 Transcription Factor

Identifiers

PMID23349490
PMCPMC3661639
OpenAlexW2170651004

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.