Evidence map›Paper›PMID 24101667›Full record

ArticleHypertension (Dallas, Tex. : 1979)2014

In vivo transfection of manganese superoxide dismutase gene or nuclear factor κB shRNA in nodose ganglia improves aortic baroreceptor function in heart failure rats.

Dongze Zhang, Jinxu Liu, Huiyin Tu, Robert L Muelleman, Kurtis G Cornish, Yu-Long Li

Open access · bronzeAbstract read
In one paragraph

Article in Hypertension (Dallas, Tex. : 1979), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.2field-weighted citation impact, top 20% 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

20 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Stellate Ganglia and Cardiac Sympathetic Overactivation in Heart Failure.International journal of molecular sciences · 2022
    Review
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  12. Review
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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.

Dongze ZhangDepartment of Emergency Medicine, University of Nebraska Medical Center, 985850 Nebraska Medical Center, Omaha, NE 68198-5850. yulongli@unmc.edu.
Jinxu Liu
Huiyin Tu
Robert L Muelleman
Kurtis G Cornish
Yu-Long Li
University of Nebraska Medical Center · US

Funding

Dysfunction of Baroreceptor Neurons in Heart Failure: Cellular and Molecular MechR01HL098503 · NHLBI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI LI, YU-LONG · 2010 to 2013
$1.5M
NHLBI NIH HHS HL-098503NHLBI NIH HHS R01 HL098503
6 · The paper itself

Abstract

Arterial baroreflex sensitivity is attenuated in chronic heart failure (CHF) state, which is associated with cardiac arrhythmias and sudden cardiac death in patients with CHF. Our previous study showed that CHF-induced sodium channel dysfunction in the baroreceptor neurons was involved in the blunted baroreflex sensitivity in CHF rats. Mitochondria-derived superoxide overproduction decreased expression and activation of the sodium channels in the baroreceptor neurons from CHF rats. However, the molecular mechanisms responsible for the sodium channel dysfunction in the baroreceptor neurons from CHF rats remain unknown. We tested the involvement of nuclear factor κB (NFκB) in the sodium channel dysfunction and evaluated the effects of in vivo transfection of manganese superoxide dismutase gene and NFκB shRNA on the baroreflex function in CHF rats. CHF was developed at 6 to 8 weeks after left coronary artery ligation in adult rats. Western blot and chromatin immunoprecipitation data showed that phosphorylated NFκB p65 and ability of NFκB p65 binding to the sodium channel promoter were increased in the nodose ganglia from CHF rats. In vivo transfection of adenoviral manganese superoxide dismutase gene or lentiviral NFκB p65 shRNA into the nodose ganglia partially reversed CHF-reduced sodium channel expression and cell excitability in the baroreceptor neurons and improved CHF-blunted arterial baroreflex sensitivity. Additionally, transfection of adenoviral manganese superoxide dismutase also inhibited the augmentation of phosphorylated NFκB p65 in the nodose neurons from CHF rats. The present study suggests that superoxide-NFκB signaling contributes to CHF-induced baroreceptor dysfunction and resultant impairment of baroreflex function.

Indexed as

AnimalsBaroreflexChronic DiseaseDisease Models, AnimalHeart FailureMaleNAV1.7 Voltage-Gated Sodium ChannelNF-kappa BNodose GanglionRatsRats, Sprague-DawleyRNA, Small InterferingSuperoxide DismutaseSuperoxidesTransfectionNAV1.7 Voltage-Gated Sodium ChannelNF-kappa BRNA, Small InterferingScn9a protein, ratSuperoxide DismutaseSuperoxidesbaroreflexheart failurepressoreceptorssodium channelssuperoxides

Identifiers

PMID24101667
PMCPMC3893036
OpenAlexW2109782683

What OpenQuestion holds

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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.