Evidence map›Paper›PMID 35725651›Full record

ArticleCell & bioscience2022

Mechanism of reduced muscle atrophy via ketone body (D)-3-hydroxybutyrate.

Jin Chen, Zihua Li, Yudian Zhang, Xu Zhang, Shujie Zhang, Zonghan Liu, Huimei Yuan, Xiangsheng Pang, Yaxuan Liu, Wuchen Tao and 3 more

Open access · goldAbstract read
In one paragraph

Article in Cell & bioscience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
6.2field-weighted citation impact, top 2% 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

19 citing papers in PubMed, 35 citations in OpenAlex.

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  14. Metabolomics-driven discovery of therapeutic targets for cancer cachexia.Journal of cachexia, sarcopenia and muscle · 2024
    Review
  15. Microbiome · 2024
    Article
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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

13 authors at 2 institutions in 1 country.

Jin ChenSchool of Life Sciences, Tsinghua University, Beijing, 100084, China.
Zihua LiSchool of Life Sciences, Tsinghua University, Beijing, 100084, China.
Yudian ZhangSchool of Life Sciences, Tsinghua University, Beijing, 100084, China.
Xu ZhangSchool of Life Sciences, Tsinghua University, Beijing, 100084, China.
Shujie ZhangSchool of Life Sciences, Tsinghua University, Beijing, 100084, China.
Zonghan LiuNational Key Laboratory of Human Factors Engineering, China Astronaut Research and Training Center, Beijing, 100094, China.
Huimei YuanNational Key Laboratory of Human Factors Engineering, China Astronaut Research and Training Center, Beijing, 100094, China.
Xiangsheng PangNational Key Laboratory of Human Factors Engineering, China Astronaut Research and Training Center, Beijing, 100094, China.
Yaxuan LiuNational Key Laboratory of Human Factors Engineering, China Astronaut Research and Training Center, Beijing, 100094, China.
Wuchen TaoNational Key Laboratory of Human Factors Engineering, China Astronaut Research and Training Center, Beijing, 100094, China.
Xiaoping ChenNational Key Laboratory of Human Factors Engineering, China Astronaut Research and Training Center, Beijing, 100094, China. xpchen2009@163.com.
Peng ZhangState Key Laboratory of Space Medicine Fundamentals and Application, China Astronaut Research and Training Center, Beijing, 100094, China. zhangpeng6128@163.com.
Guo-Qiang ChenSchool of Life Sciences, Tsinghua University, Beijing, 100084, China. chengq@mail.tsinghua.edu.cn.ORCID http://orcid.org/0000-0002-7226-1782
China Astronaut Research and Training Center · CNTsinghua University · CN

Funding

Chunfeng Foundation 2020Z99CFG002National Natural Science Foundation of China 32171173Open Funding Project of National Key Laboratory of Human Factors Engineering 6142222200106
6 · The paper itself

Abstract

backgroundMuscle atrophy is an increasingly global health problem affecting millions, there is a lack of clinical drugs or effective therapy. Excessive loss of muscle mass is the typical characteristic of muscle atrophy, manifesting as muscle weakness accompanied by impaired metabolism of protein and nucleotide. (D)-3-hydroxybutyrate (3HB), one of the main components of the ketone body, has been reported to be effective for the obvious hemodynamic effects in atrophic cardiomyocytes and exerts beneficial metabolic reprogramming effects in healthy muscle. This study aims to exploit how the 3HB exerts therapeutic effects for treating muscle atrophy induced by hindlimb unloaded mice.

resultsAnabolism/catabolism balance of muscle protein was maintained with 3HB via the Akt/FoxO3a and the mTOR/4E-BP1 pathways; protein homeostasis of 3HB regulation includes pathways of ubiquitin-proteasomal, autophagic-lysosomal, responses of unfolded-proteins, heat shock and anti-oxidation. Metabolomic analysis revealed the effect of 3HB decreased purine degradation and reduced the uric acid in atrophied muscles; enhanced utilization from glutamine to glutamate also provides evidence for the promotion of 3HB during the synthesis of proteins and nucleotides.

conclusions3HB significantly inhibits the loss of muscle weights, myofiber sizes and myofiber diameters in hindlimb unloaded mouse model; it facilitates positive balance of proteins and nucleotides with enhanced accumulation of glutamate and decreased uric acid in wasting muscles, revealing effectiveness for treating muscle atrophy.

Indexed as

3-HydroxybutyrateGlutamineKetone BodyMetabolomicsMuscle atrophyNucleotide synthesisProtein

Identifiers

PMID35725651
PMCPMC9208164
OpenAlexW4283163434

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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.