Evidence map›Paper›PMID 22933112›Full record

ArticleDiabetes2012

Altered MAPK signaling in progressive deterioration of endothelial function in diabetic mice.

An Huang, Yang-Ming Yang, Changdong Yan, Gabor Kaley, Thomas H Hintze, Dong Sun

Open access · hybridAbstract read
In one paragraph

Article in Diabetes, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

26 citing papers in PubMed, 45 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Review
  6. Review
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  9. Review
  10. Article
  11. Article
  12. Article
  13. Microvascular NADPH oxidase in health and disease.Free radical biology & medicine · 2017
    Review
  14. Divergent outcomes of fructose consumption on exercise capacity of rats: friend or foe.Journal of applied physiology (Bethesda, Md. : 1985) · 2017
    Article
  15. Article
  16. Article
  17. Article
  18. Role of homocysteinylation of ACE in endothelial dysfunction of arteries.American journal of physiology. Heart and circulatory physiology · 2015
    Article
  19. 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

6 authors at 2 institutions in 2 countries.

An HuangDepartment of Physiology, New York Medical College, Valhalla, New York, USA. an_huang@nymc.edu
Yang-Ming Yang
Changdong Yan
Gabor Kaley
Thomas H Hintze
Dong Sun
New York Medical College · USXuzhou Medical College · CN

Funding

VASCULAR REGULATION BY FLOW VELOCITY/ENDOTHELIUMP01HL043023 · NHLBI · NEW YORK MEDICAL COLLEGE · PI KALEY, GABOR · 1991 to 2011
$19.5M
Estrogen and EDHF in NO DeficiencyR01HL070653 · NHLBI · NEW YORK MEDICAL COLLEGE · PI HUANG, AN · 2003 to 2017
$3.7M
NHLBI NIH HHS HL-070653NHLBI NIH HHS HL-43023NHLBI NIH HHS P01 HL043023NHLBI NIH HHS R01 HL070653
6 · The paper itself

Abstract

We aimed to investigate specific roles of mitogen-activated protein kinases (MAPK) in the deterioration of endothelial function during the progression of diabetes and the potential therapeutic effects of MAPK inhibitors and agonists in the amelioration of endothelial function. Protein expression and phosphorylation of p38, c-Jun NH(2)-terminal kinase (JNK), and extracellular signal-regulated kinase (Erk) were assessed in mesenteric arteries of 3- (3M) and 9-month-old (9M) male diabetic and control mice. The expression of p38, JNK, and Erk was comparable in all groups of mice, but the phosphorylation of p38 and JNK was increased in 3M and further increased in 9M diabetic mice, whereas the phosphorylation of Erk was substantially reduced in 9M diabetic mice. NADPH oxidase-dependent superoxide production was significantly increased in vessels of two ages of diabetic mice. Inhibition of either p38 with SB203580 or JNK with SP600125 reduced superoxide production and improved shear stress-induced dilation (SSID) in 3M, but not in 9M, diabetic mice. Treating the vessels of 9M diabetic mice with resveratrol increased Erk phosphorylation and shear stress-induced endothelial nitric oxide synthase (eNOS) phosphorylation and activity, but resveratrol alone did not improve SSID. Administration of resveratrol and SB203580 or resveratrol and SP600125 together significantly improved SSID in vessels of 9M diabetic mice. The improved response was prevented by U0126, an Erk inhibitor. Thus, p38/JNK-dependent increase in oxidative stress diminished nitric oxide-mediated dilation in vessels of 3M diabetic mice. Oxidative stress and impaired Erk-dependent activation of eNOS exacerbates endothelial dysfunction in the advanced stage of diabetes.

Indexed as

AnimalsAnthracenesButadienesDiabetes Mellitus, Type 2Extracellular Signal-Regulated MAP KinasesImidazolesImmunoblottingJNK Mitogen-Activated Protein KinasesMaleMiceMitogen-Activated Protein KinasesNitrilesOxidative Stressp38 Mitogen-Activated Protein KinasesPhosphorylationPyridinesAnthracenesButadienesExtracellular Signal-Regulated MAP KinasesImidazolesJNK Mitogen-Activated Protein Kinasesleptin receptor, mouseMitogen-Activated Protein KinasesNitrilesp38 Mitogen-Activated Protein KinasespyrazolanthronePyridinesReceptors, LeptinResveratrolSB 203580StilbenesSuperoxidesU 0126

Identifiers

PMID22933112
PMCPMC3501862
OpenAlexW2161387133

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.