Evidence mapPaperPMID 39334864Full record

ArticleBiomolecules2024

Inhibition of MAT2A Impairs Skeletal Muscle Repair Function.

Wanli Xiao, Tian-E Huang, Jing Zhou, Benhui Wang, Xiang Wang, Weirong Zeng, Qiquan Wang, Xinqiang Lan, Yang Xiang

Abstract read
In one paragraph

Article in Biomolecules, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
field-weighted citation impact
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

5 citing papers in PubMed.

  1. Silencing of MAT2A inhibits gastric cancer cell proliferation, migration, and invasion through activation of the p53 pathway.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
    Article
  2. Article
  3. Review
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  5. Article
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

9 authors.

Wanli XiaoMetabolic Control and Aging-Jiangxi Key Laboratory of Aging and Diseases, Human Aging Research Institute (HARI), School of Life Science, Nanchang University, Nanchang 330031, China.
Tian-E HuangMetabolic Control and Aging-Jiangxi Key Laboratory of Aging and Diseases, Human Aging Research Institute (HARI), School of Life Science, Nanchang University, Nanchang 330031, China.
Jing ZhouMetabolic Control and Aging-Jiangxi Key Laboratory of Aging and Diseases, Human Aging Research Institute (HARI), School of Life Science, Nanchang University, Nanchang 330031, China.
Benhui WangMetabolic Control and Aging-Jiangxi Key Laboratory of Aging and Diseases, Human Aging Research Institute (HARI), School of Life Science, Nanchang University, Nanchang 330031, China.
Xiang WangMetabolic Control and Aging-Jiangxi Key Laboratory of Aging and Diseases, Human Aging Research Institute (HARI), School of Life Science, Nanchang University, Nanchang 330031, China.
Weirong ZengMetabolic Control and Aging-Jiangxi Key Laboratory of Aging and Diseases, Human Aging Research Institute (HARI), School of Life Science, Nanchang University, Nanchang 330031, China.
Qiquan WangMetabolic Control and Aging-Jiangxi Key Laboratory of Aging and Diseases, Human Aging Research Institute (HARI), School of Life Science, Nanchang University, Nanchang 330031, China.
Xinqiang LanMetabolic Control and Aging-Jiangxi Key Laboratory of Aging and Diseases, Human Aging Research Institute (HARI), School of Life Science, Nanchang University, Nanchang 330031, China.
Yang XiangMetabolic Control and Aging-Jiangxi Key Laboratory of Aging and Diseases, Human Aging Research Institute (HARI), School of Life Science, Nanchang University, Nanchang 330031, China.ORCID 0000-0003-3016-0323

Funding

Jiangxi Province 20181BCD40001Jiangxi Province 20192BCB23004Jiangxi Province 20221ZDG020070Jiangxi Province 2024SSY07161Jiangxi Province jxsq2018106036Nanchang University 28740105National Key R&D Program, Ministry of Science and Technology of China 2020YFC2002900National Key R&D Program, Ministry of Science and Technology of China 2023YFC3603300National Key R&D Program, Ministry of Science and Technology of China 2023YFF1001000National Natural Science Foundation of China 81873814National Natural Science Foundation of China 82330046
6 · The paper itself

Abstract

The regenerative capacity of muscle, which primarily relies on anabolic processes, diminishes with age, thereby reducing the effectiveness of therapeutic interventions aimed at treating age-related muscle atrophy. In this study, we observed a decline in the expression of methionine adenosine transferase 2A (MAT2A), which synthesizes S-adenosylmethionine (SAM), in the muscle tissues of both aged humans and mice. Considering MAT2A's critical role in anabolism, we hypothesized that its reduced expression contributes to the impaired regenerative capacity of aging skeletal muscle. Mimicking this age-related reduction in the MAT2A level, either by reducing gene expression or inhibiting enzymatic activity, led to inhibiting their differentiation into myotubes.

Indexed as

Methionine AdenosyltransferaseMuscle, SkeletalAgedAgingAnimalsApoptosisCell DifferentiationCell Linefas ReceptorHumansMaleMiceMice, Inbred C57BLMuscle Fibers, SkeletalRegenerationS-AdenosylmethionineFas protein, mousefas ReceptorMAT2A protein, humanMethionine AdenosyltransferaseS-AdenosylmethionineTumor Suppressor Protein p53C2C12FasMat2aregenerationskeletal muscle

Identifiers

PMID39334864
PMCPMC11430595

What Socratic holds

Textmetadata
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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 Socratic graph.