Evidence map›Paper›PMID 31853045›Full record

ArticleHypertension research : official journal of the Japanese Society of Hypertension2020

Different effects of the deletion of angiotensin converting enzyme 2 and chronic activation of the renin-angiotensin system on muscle weakness in middle-aged mice.

Hikari Takeshita, Koichi Yamamoto, Masaki Mogi, Satoko Nozato, Masatsugu Horiuchi, Hiromi Rakugi

Abstract read
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In one paragraph

Article in Hypertension research : official journal of the Japanese Society of Hypertension, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.0field-weighted citation impact, top 23% 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

11 citing papers in PubMed, 17 citations in OpenAlex.

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  9. ACE2, angiotensin 1-7 and skeletal muscle: review in the era of COVID-19.Clinical science (London, England : 1979) · 2020
    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 2 institutions in 1 country.

Hikari TakeshitaDepartment of Geriatric and General Medicine, Osaka University Graduate School of Medicine, Suita, Osaka, Japan.
Koichi YamamotoDepartment of Geriatric and General Medicine, Osaka University Graduate School of Medicine, Suita, Osaka, Japan. kyamamoto@geriat.med.osaka-u.ac.jp.
Masaki MogiDepartment of Pharmacology, Ehime University Graduate School of Medicine, Toon, Ehime, Japan.
Satoko NozatoDepartment of Geriatric and General Medicine, Osaka University Graduate School of Medicine, Suita, Osaka, Japan.
Masatsugu HoriuchiDepartment of Molecular Cardiovascular Biology and Pharmacology, Ehime University, Graduate School of Medicine, Toon, Ehime, Japan.
Hiromi RakugiDepartment of Geriatric and General Medicine, Osaka University Graduate School of Medicine, Suita, Osaka, Japan.
Osaka University · JPEhime University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Inhibition of the renin-angiotensin system (RAS) has been shown to alleviate muscle atrophy both under pathological conditions and during physiological aging. We recently reported that the deletion of angiotensin converting enzyme 2 (ACE2), which converts Angiotensin II to Angiotensin-(1-7) in mice, leads to the early manifestation of aging-associated muscle weakness along with the increased expression of p16

Indexed as

AdiposityAgingAngiotensin-Converting Enzyme 2AnimalsHand StrengthHypertensionMiceMice, KnockoutMuscle, SkeletalMuscle WeaknessRenin-Angiotensin SystemAngiotensin-Converting Enzyme 2ACE2angiotensin IIRenin-angiotensin systemSarcopeniaSkeletal muscle

Identifiers

PMID31853045
OpenAlexW2996679512

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.