Evidence map›Paper›PMID 26571361›Full record

ArticleScientific reports2015

Angiotensin II receptor blockade promotes repair of skeletal muscle through down-regulation of aging-promoting C1q expression.

Chizuru Yabumoto, Hiroshi Akazawa, Rie Yamamoto, Masamichi Yano, Yoko Kudo-Sakamoto, Tomokazu Sumida, Takehiro Kamo, Hiroki Yagi, Yu Shimizu, Akiko Saga-Kamo and 7 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
1.8field-weighted citation impact, top 14% 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

32 citing papers in PubMed, 52 citations in OpenAlex.

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

17 authors at 4 institutions in 1 country.

Chizuru YabumotoDepartment of Cardiovascular Medicine, Osaka University Graduate School of Medicine, Suita, Osaka 565-0871, Japan.
Hiroshi AkazawaDepartment of Cardiovascular Medicine, Graduate School of Medicine, The University of Tokyo, Bunkyo-ku, Tokyo 113-8655, Japan.
Rie YamamotoDepartment of Cardiovascular Medicine, Chiba University Graduate School of Medicine, Chiba, Chiba 260-8670, Japan.
Masamichi YanoDepartment of Cardiovascular Medicine, Osaka University Graduate School of Medicine, Suita, Osaka 565-0871, Japan.
Yoko Kudo-SakamotoDepartment of Cardiovascular Medicine, Osaka University Graduate School of Medicine, Suita, Osaka 565-0871, Japan.
Tomokazu SumidaDepartment of Cardiovascular Medicine, Graduate School of Medicine, The University of Tokyo, Bunkyo-ku, Tokyo 113-8655, Japan.
Takehiro KamoDepartment of Cardiovascular Medicine, Graduate School of Medicine, The University of Tokyo, Bunkyo-ku, Tokyo 113-8655, Japan.
Hiroki YagiDepartment of Cardiovascular Medicine, Graduate School of Medicine, The University of Tokyo, Bunkyo-ku, Tokyo 113-8655, Japan.
Yu ShimizuDepartment of Cardiovascular Medicine, Graduate School of Medicine, The University of Tokyo, Bunkyo-ku, Tokyo 113-8655, Japan.
Akiko Saga-KamoDepartment of Cardiovascular Medicine, Graduate School of Medicine, The University of Tokyo, Bunkyo-ku, Tokyo 113-8655, Japan.
Atsuhiko T NaitoDepartment of Cardiovascular Medicine, Osaka University Graduate School of Medicine, Suita, Osaka 565-0871, Japan.
Toru OkaDepartment of Cardiovascular Medicine, Osaka University Graduate School of Medicine, Suita, Osaka 565-0871, Japan.
Jong-Kook LeeDepartment of Cardiovascular Regenerative Medicine, Osaka University Graduate School of Medicine, Suita, Osaka 565-0871, Japan.
Jun-Ichi SuzukiDepartment of Advanced Clinical Science and Therapeutics, Graduate School of Medicine, The University of Tokyo, Bunkkyo-ku, Tokyo 113-8655, Japan.
Yasushi SakataDepartment of Cardiovascular Medicine, Osaka University Graduate School of Medicine, Suita, Osaka 565-0871, Japan.
Etsuko UejimaClinical Pharmacy Education Unit, Graduate School of Pharmaceutical Sciences, Osaka University, Suita, Osaka 565-0871, Japan.
Issei KomuroDepartment of Cardiovascular Medicine, Graduate School of Medicine, The University of Tokyo, Bunkyo-ku, Tokyo 113-8655, Japan.
The University of Tokyo · JPOsaka University · JPJapan Agency for Medical Research and Development · JPChiba University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Disruption of angiotensin II type 1 (AT1) receptor prolonged life span in mice. Since aging-related decline in skeletal muscle function was retarded in Atgr1a(-/-) mice, we examined the role of AT1 receptor in muscle regeneration after injury. Administration of AT1 receptor blocker irbesartan increased the size of regenerating myofibers, decreased fibrosis, and enhanced functional muscle recovery after cryoinjury. We recently reported that complement C1q, secreted by macrophages, activated Wnt/β-catenin signaling and promoted aging-related decline in regenerative capacity of skeletal muscle. Notably, irbesartan induced M2 polarization of macrophages, but reduced C1q expression in cryoinjured muscles and in cultured macrophage cells. Irbesartan inhibited up-regulation of Axin2, a downstream gene of Wnt/β-catenin pathway, in cryoinjured muscles. In addition, topical administration of C1q reversed beneficial effects of irbesartan on skeletal muscle regeneration after injury. These results suggest that AT1 receptor blockade improves muscle repair and regeneration through down-regulation of the aging-promoting C1q-Wnt/β-catenin signaling pathway.

Indexed as

Administration, TopicalAgingAngiotensin II Type 1 Receptor BlockersAnimalsAxin ProteinBiphenyl CompoundsCell LineComplement C1qDown-RegulationImmunohistochemistryIrbesartanMacrophagesMaleMiceMice, Inbred C57BLMice, KnockoutAngiotensin II Type 1 Receptor BlockersAxin2 protein, mouseAxin ProteinBiphenyl CompoundsComplement C1qIrbesartanPax7 protein, mousePAX7 Transcription FactorReceptor, Angiotensin, Type 1Tetrazoles

Identifiers

PMID26571361
PMCPMC4585890
OpenAlexW2410812192

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.