Evidence map›Paper›PMID 29230587›Full record

ArticleClinical and experimental nephrology2018

Arterial wall hypertrophy is ameliorated by α2-adrenergic receptor antagonist or aliskiren in kidneys of angiotensinogen-knockout mice.

Haruka Nakamori, Shin-Ichiro Yoshida, Hiroaki Ishiguro, Shota Suzuki, Hiroaki Yasuzaki, Tatsuo Hashimoto, Tomoaki Ishigami, Nobuhito Hirawa, Yoshiyuki Toya, Satoshi Umemura and 1 more

Abstract read
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Article in Clinical and experimental nephrology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.2field-weighted citation impact, top 40% 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

3 citing papers in PubMed, 5 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
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

11 authors at 1 institution in 1 country.

Haruka Nakamori *Department of Medical Science and Cardiorenal Medicine, Yokohama City University Graduate School of Medicine, 3-9 Fukuura, Kanazawa-ku, Yokohama, 236-0004, Japan.
Shin-Ichiro Yoshida *Department of Medical Science and Cardiorenal Medicine, Yokohama City University Graduate School of Medicine, 3-9 Fukuura, Kanazawa-ku, Yokohama, 236-0004, Japan. yoshidas@yokohama-cu.ac.jp.ORCID http://orcid.org/0000-0003-3728-6412
Hiroaki IshiguroDepartment of Medical Science and Cardiorenal Medicine, Yokohama City University Graduate School of Medicine, 3-9 Fukuura, Kanazawa-ku, Yokohama, 236-0004, Japan.
Shota SuzukiDepartment of Medical Science and Cardiorenal Medicine, Yokohama City University Graduate School of Medicine, 3-9 Fukuura, Kanazawa-ku, Yokohama, 236-0004, Japan.
Hiroaki YasuzakiDepartment of Medical Science and Cardiorenal Medicine, Yokohama City University Graduate School of Medicine, 3-9 Fukuura, Kanazawa-ku, Yokohama, 236-0004, Japan.
Tatsuo HashimotoDepartment of Medical Science and Cardiorenal Medicine, Yokohama City University Graduate School of Medicine, 3-9 Fukuura, Kanazawa-ku, Yokohama, 236-0004, Japan.
Tomoaki IshigamiDepartment of Medical Science and Cardiorenal Medicine, Yokohama City University Graduate School of Medicine, 3-9 Fukuura, Kanazawa-ku, Yokohama, 236-0004, Japan.
Nobuhito HirawaDepartment of Medical Science and Cardiorenal Medicine, Yokohama City University Graduate School of Medicine, 3-9 Fukuura, Kanazawa-ku, Yokohama, 236-0004, Japan.
Yoshiyuki ToyaDepartment of Medical Science and Cardiorenal Medicine, Yokohama City University Graduate School of Medicine, 3-9 Fukuura, Kanazawa-ku, Yokohama, 236-0004, Japan.
Satoshi UmemuraDepartment of Medical Science and Cardiorenal Medicine, Yokohama City University Graduate School of Medicine, 3-9 Fukuura, Kanazawa-ku, Yokohama, 236-0004, Japan.
Kouichi TamuraDepartment of Medical Science and Cardiorenal Medicine, Yokohama City University Graduate School of Medicine, 3-9 Fukuura, Kanazawa-ku, Yokohama, 236-0004, Japan.
Yokohama City University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundArterial hypertrophy and interstitial fibrosis are important characteristics in kidneys of angiotensinogen-knockout (Atg

methodsWe performed renal denervation and administered the α2-adrenergic receptor (AR) antagonist, atipamezole, to Atg

resultsNorepinephrine content in kidneys of Atg

conclusionsAlpha2-AR signaling is one of the causes of persistent renal arterial hypertrophy in Atg

Indexed as

Adrenergic alpha-2 Receptor AntagonistsAmidesAngiotensinogenAnimalsFibrosisFumaratesHypertrophyJapanKidneyMiceMice, Inbred ICRMice, KnockoutRenal ArteryReninTokyoTransforming Growth Factor beta1Adrenergic alpha-2 Receptor AntagonistsaliskirenAmidesAngiotensinogenFumaratesReninTransforming Growth Factor beta1AliskirenAngiotensinogen-knockout mouseArterial hypertrophyKidneySympathetic nerve

Identifiers

PMID29230587
OpenAlexW2772266883

What OpenQuestion holds

Textmetadata
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.