Evidence map›Paper›PMID 37759480›Full record

ArticleCells2023

Silk Peptide Ameliorates Sarcopenia through the Regulation of Akt/mTOR/FoxO3a Signaling Pathways and the Inhibition of Low-Grade Chronic Inflammation in Aged Mice.

Hyun-Ji Oh, Heegu Jin, Jeong-Yong Lee, Boo-Yong Lee

Open access · goldAbstract read
In one paragraph

Article in Cells, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

8 citing papers in PubMed, 13 citations in OpenAlex.

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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

4 authors at 1 institution in 1 country.

Hyun-Ji OhDepartment of Food Science and Biotechnology, College of Life Science, CHA University, Seongnam 13488, Republic of Korea.
Heegu JinDepartment of Food Science and Biotechnology, College of Life Science, CHA University, Seongnam 13488, Republic of Korea.
Jeong-Yong LeeWorldway Co., Ltd., Sejong 30003, Republic of Korea.
Boo-Yong LeeDepartment of Food Science and Biotechnology, College of Life Science, CHA University, Seongnam 13488, Republic of Korea.
CHA University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

As populations around the world age, interest in healthy aging is growing. One of the first physical changes that occurs with aging is the loss of muscle mass and strength, termed sarcopenia. Sarcopenia limits the activity of older people, reduces their quality of life, and increases the likelihood of their developing disease. In the present study, we aimed to evaluate the effects of the ingestion of acid-hydrolyzed silk peptide (SP) on the muscle mass and strength of mice of >22 months of age with naturally occurring sarcopenia, and to identify the mechanisms involved. The daily administration of SP for 8 weeks increased the activation of the Akt/mTOR/FoxO3a signaling pathways and increased the muscle mass and strength of the old mice. In addition, SP inhibited oxidative stress and inflammation in muscle, which are direct causes of sarcopenia. Therefore, SP represents a promising potential treatment for sarcopenia that may improve the healthy lifespan and quality of life of older people.

Indexed as

Proto-Oncogene Proteins c-aktSarcopeniaAgedAnimalsHumansInflammationMicePeptidesQuality of LifeSignal TransductionSilkTOR Serine-Threonine KinasesPeptidesProto-Oncogene Proteins c-aktSilkTOR Serine-Threonine Kinasesacid-hydrolyzed silk peptideagingAktFoxO3ainflammationmTORoxidative stresssarcopeniasignaling pathway

Identifiers

PMID37759480
PMCPMC10527450
OpenAlexW4386645063

What Socratic 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 Socratic graph.