Evidence map›Paper›PMID 25028667›Full record

ArticleBioMed research international2014

Adrenomedullin deficiency and aging exacerbate ischemic white matter injury after prolonged cerebral hypoperfusion in mice.

Yumiko Mitome-Mishima, Nobukazu Miyamoto, Ryota Tanaka, Tatsuo Shimosawa, Hidenori Oishi, Hajime Arai, Nobutaka Hattori, Takao Urabe

Open access · hybridAbstract read
In one paragraph

Article in BioMed research international, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing 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

9 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
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  4. Endogenous Vasoactive Peptides and Vascular Aging-Related Diseases.Oxidative medicine and cellular longevity · 2022
    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

8 authors at 3 institutions in 1 country.

Yumiko Mitome-MishimaDepartment of Neurosurgery, Juntendo University School of Medicine, Tokyo, Japan.
Nobukazu MiyamotoDepartment of Neurology, Juntendo University Urayasu Hospital, 2-1-1 Tomioka, Urayasu, Chiba 279-0021, Japan.
Ryota TanakaDepartment of Neurology, Juntendo University School of Medicine, Tokyo, Japan.
Tatsuo ShimosawaDepartment of Clinical Laboratory, Faculty of Medicine, The University of Tokyo, Tokyo, Japan.
Hidenori OishiDepartment of Neurosurgery, Juntendo University School of Medicine, Tokyo, Japan ; Department of Neuroendovascular Therapy, Juntendo University School of Medicine, Tokyo, Japan.
Hajime AraiDepartment of Neurosurgery, Juntendo University School of Medicine, Tokyo, Japan.
Nobutaka HattoriDepartment of Neurology, Juntendo University School of Medicine, Tokyo, Japan.
Takao UrabeDepartment of Neurology, Juntendo University Urayasu Hospital, 2-1-1 Tomioka, Urayasu, Chiba 279-0021, Japan.
Juntendo University · JPJuntendo University Urayasu Hospital · JPThe University of Tokyo · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Adrenomedullin was originally isolated from pheochromocytoma cells and reduces insulin resistance by decreasing oxidative stress. White matter lesions induced by aging and hyperglycemia play a crucial role in cognitive impairment in poststroke patients. Here, we examine whether adrenomedullin deficiency and aging exacerbate ischemic white matter injury after prolonged cerebral hypoperfusion. Adrenomedullin heterozygous, wild-type young/aged mice were subjected to prolonged hypoperfusion. Prolonged cerebral hypoperfusion followed by immunohistochemical analysis was used to evaluate white matter injury. After prolonged hypoperfusion, white matter damage progressed in a time-dependent manner in AM(+/-) group compared with the wild-type group. The number of oligodendrocyte progenitor cells gradually increased after prolonged hypoperfusion, whereas oligodendrocytes decreased following a transient increase, but the ratio of increase was mild in the AM(+/-) group (P < 0.05). Oxidative stress was detected in oligodendrocytes, with a larger increase in the AM(+/-) group (P < 0.05). Aged mice showed the same tendency, but white matter damage was worse, especially in the aged AM(+/-) group. Our results demonstrated that white matter injury was increased in adrenomedullin deficiency, which induced oxidative stress. White matter injury was more exacerbated because of hyperglycemia in aged AM(+/-) group. Adrenomedullin may be an important target in the control of ischemic white matter injury.

Indexed as

AdrenomedullinAgingAnimalsChronic DiseaseHypoxia-Ischemia, BrainMaleMiceMice, Mutant StrainsNeural Stem CellsOligodendrogliaWhite MatterAdrenomedullin

Identifiers

PMID25028667
PMCPMC4084515
OpenAlexW2043595907

What OpenQuestion holds

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LicenceCC BY
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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.