Evidence map›Paper›PMID 39761956›Full record

ArticlePhysiological reports2025

miRNA-1 regulation is necessary for mechanical overload-induced muscle hypertrophy in male mice.

Shengyi Fei, Blake D Rule, Joshua S Godwin, C Brooks Mobley, Michael D Roberts, Ferdinand von Walden, Ivan J Vechetti

Abstract read
In one paragraph

Article in Physiological reports, 2025. 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
–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

8 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Muscle memory theory: A critical evaluation.The Journal of physiology · 2025
    Article
  6. Review
  7. Review
  8. 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

7 authors.

Shengyi FeiDepartment of Nutrition and Health Sciences, University of Nebraska-Lincoln, Lincoln, Nebraska, USA.
Blake D RuleDepartment of Nutrition and Health Sciences, University of Nebraska-Lincoln, Lincoln, Nebraska, USA.
Joshua S GodwinSchool of Kinesiology, Auburn University, Auburn, Alabama, USA.
C Brooks MobleySchool of Kinesiology, Auburn University, Auburn, Alabama, USA.
Michael D RobertsSchool of Kinesiology, Auburn University, Auburn, Alabama, USA.ORCID https://orcid.org/0000-0002-7359-5362
Ferdinand von WaldenDepartment of Women's and Children's Health, Karolinska Institutet, Stockholm, Sweden.ORCID https://orcid.org/0000-0003-1134-2252
Ivan J VechettiDepartment of Nutrition and Health Sciences, University of Nebraska-Lincoln, Lincoln, Nebraska, USA.ORCID https://orcid.org/0000-0003-1024-1011

Funding

The role of stress in the fetal origin of obesity and metabolic dysfunctionP20GM104320 · NIGMS · UNIVERSITY OF NEBRASKA LINCOLN · PI ZEMPLENI, JANOS · 2014 to 2024
$24.9M
Åke Wiberg FoundationHHS | NIH | National Institute of General Medical Sciences (NIGMS) P20GM104320-07NIGMS NIH HHS P20 GM104320Swedish Medical Association SLS-986170Swedish research council 2022-01392Swedish Research Council for Sport Science 2022/10'Swedish Research Council for Sport Science '2023/09
6 · The paper itself

Abstract

MicroRNAs (miRNAs) are small, noncoding RNAs that play a critical role in regulating gene expression post-transcriptionally. They are involved in various developmental and physiological processes, and their dysregulation is linked to various diseases. Skeletal muscle-specific miRNAs, including miR-1, play a crucial role in the development and maintenance of skeletal muscle. It has been demonstrated that the expression of miR-1 decreases by approximately 50% in response to hypertrophic stimuli, suggesting its potential involvement in muscle hypertrophy. In our study, we hypothesize that reduction of miR-1 levels is necessary for skeletal muscle growth due to its interaction to essential pro-growth genes. Promoting a smaller reduction of miR-1 levels, we observed a blunted hypertrophic response in mice undergoing a murine model of muscle hypertrophy. In addition, our results suggest that miR-1 inhibits the expression of Itm2a, a membrane-related protein, as potential miR-1-related candidate for skeletal muscle hypertrophy. While the exact mechanism in muscle hypertrophy has not been identified, our results suggest that miR-1-regulated membrane proteins are important for skeletal muscle hypertrophy.

Indexed as

HypertrophyMice, Inbred C57BLMicroRNAsMuscle, SkeletalAnimalsMaleMiceMicroRNAsMirn1 microRNA, mousehypertrophymiR‐1skeletal muscle

Identifiers

PMID39761956
PMCPMC11705529

What Socratic holds

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Registered trials

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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 Socratic graph.