Evidence map›Paper›PMID 24631774›Full record

ArticleJournal of molecular and cellular cardiology2014

Nox2 mediates high fat high sucrose diet-induced nitric oxide dysfunction and inflammation in aortic smooth muscle cells.

Zhexue Qin, Xiuyun Hou, Robert M Weisbrod, Francesca Seta, Richard A Cohen, Xiaoyong Tong

Abstract read
In one paragraph

Article in Journal of molecular and cellular cardiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.9field-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

16 citing papers in PubMed, 33 citations in OpenAlex.

  1. Review
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  6. Inactivation of CysBritish journal of pharmacology · 2020
    Article
  7. Review
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  10. Obesity-induced vascular inflammation involves elevated arginase activity.American journal of physiology. Regulatory, integrative and comparative physiology · 2017
    Article
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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

6 authors at 1 institution in 1 country.

Zhexue QinVascular Biology Section, Department of Medicine, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, MA 02118, USA; Department of Cardiovascular Diseases, Xinqiao Hospital, Third Military Medical University, Chongqing 400037, China.
Xiuyun HouVascular Biology Section, Department of Medicine, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, MA 02118, USA.
Robert M WeisbrodVascular Biology Section, Department of Medicine, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, MA 02118, USA.
Francesca SetaVascular Biology Section, Department of Medicine, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, MA 02118, USA.
Richard A CohenVascular Biology Section, Department of Medicine, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, MA 02118, USA.
Xiaoyong TongVascular Biology Section, Department of Medicine, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, MA 02118, USA. Electronic address: xytong@bu.edu.
Boston University · US

Funding

Redox Regulation of SERCA by Nitric OxideR01HL031607 · NHLBI · BOSTON UNIVERSITY MEDICAL CENTER HOSP · PI COHEN, RICHARD A · 1985 to 2013
$4.8M
Redox Regulation of p21ras in AngiogenesisR37HL104017 · NHLBI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI COHEN, RICHARD A · 2010 to 2014
$2.2M
Aortic Stiffness and Hypertension in Obese MiceR01HL105287 · NHLBI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI COHEN, RICHARD A · 2010 to 2013
$1.6M
NHLBI NIH HHS R01 HL031607NHLBI NIH HHS R01 HL105287NHLBI NIH HHS R37 HL104017
6 · The paper itself

Abstract

Diet-induced obesity and metabolic syndrome are important contributors to cardiovascular diseases. The decreased nitric oxide (NO) bioactivity in endothelium and the impaired response of smooth muscle cell (SMC) to NO significantly contribute to vascular pathologies, including atherosclerosis and arterial restenosis after angioplasty. Sarco/endoplasmic reticulum Ca(2+) ATPase (SERCA) is an important mediator of NO function in both endothelial cells and SMCs, and its irreversible oxidation impairs its stimulation by NO. We used C57BL/6J mice fed a high fat high sucrose diet (HFHSD) to study the role of SMC SERCA in diet-induced obesity and metabolic syndrome. We found that HFHSD upregulated Nox2 based NADPH oxidase, induced inflammation, increased irreversible SERCA oxidation, and suppressed the response of aortic SERCA to NO. Cultured aortic SMCs from mice fed HFHSD showed increased reactive oxygen species production, Nox2 upregulation, irreversible SERCA oxidation, inflammation, and a decreased ability of NO to inhibit SMC migration. Overexpression of wild type SERCA2b or downregulation of Nox2 restored NO-mediated inhibition of migration in SMCs isolated from HFHSD-fed mice. In addition, tumor necrosis factor alpha (TNFα) increased Nox2 which induced SERCA oxidation and inflammation. Taken together, Nox2 induced by HFHSD plays significant roles in controlling SMC responses to NO and TNFα-mediated inflammation, which may contribute to the development of cardiovascular diseases in diet-induced obesity and metabolic syndrome.

Indexed as

AnimalsAortaCell MovementDiet, High-FatEndothelium, VascularGene Expression RegulationInflammationMaleMembrane GlycoproteinsMetabolic SyndromeMiceMice, Inbred C57BLMyocytes, Smooth MuscleNADPH Oxidase 2NADPH OxidasesNitric OxideAtp2a2 protein, mouseCybb protein, mouseMembrane GlycoproteinsNADPH Oxidase 2NADPH OxidasesNitric OxideReactive Oxygen SpeciesSarcoplasmic Reticulum Calcium-Transporting ATPasesSucroseTumor Necrosis Factor-alphaHigh fat high sucrose dietNitric oxideNox2Sarco/endoplasmic reticulum Ca(2+) ATPaseSmooth muscle cell

Identifiers

PMID24631774
PMCPMC4037381
OpenAlexW2059654432

What OpenQuestion holds

Textmetadata
LicenceTDM
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.