Evidence map›Paper›PMID 35155444›Full record

ArticleFrontiers in cell and developmental biology2021

Myostatin Mutation Promotes Glycolysis by Increasing Phosphorylation of Phosphofructokinase

Mingjuan Gu, Xinyu Zhou, Lin Zhu, Yajie Gao, Li Gao, Chunling Bai, Lei Yang, Guangpeng Li

Open access · goldAbstract read
In one paragraph

Article in Frontiers in cell and developmental biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.1field-weighted citation impact, top 24% 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

10 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Loss ofCurrent issues in molecular biology · 2025
    Article
  5. Unveiling the functions of five recently characterized lncRNAs in cancer progression.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025
    Review
  6. Article
  7. Phosphodiesterase 5a Signalling in Skeletal Muscle Pathophysiology.International journal of molecular sciences · 2022
    Article
  8. Article
  9. Article
  10. Review
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

8 authors at 2 institutions in 1 country.

Mingjuan GuState Key Laboratory of Reproductive Regulation and Breeding of Grassland Livestock, Inner Mongolia University, Hohhot, China.
Xinyu ZhouState Key Laboratory of Reproductive Regulation and Breeding of Grassland Livestock, Inner Mongolia University, Hohhot, China.
Lin ZhuState Key Laboratory of Reproductive Regulation and Breeding of Grassland Livestock, Inner Mongolia University, Hohhot, China.
Yajie GaoState Key Laboratory of Reproductive Regulation and Breeding of Grassland Livestock, Inner Mongolia University, Hohhot, China.
Li GaoBaotou Teachers' College, Baotou, China.
Chunling BaiState Key Laboratory of Reproductive Regulation and Breeding of Grassland Livestock, Inner Mongolia University, Hohhot, China.
Lei YangState Key Laboratory of Reproductive Regulation and Breeding of Grassland Livestock, Inner Mongolia University, Hohhot, China.
Guangpeng LiState Key Laboratory of Reproductive Regulation and Breeding of Grassland Livestock, Inner Mongolia University, Hohhot, China.
Inner Mongolia University · CNBaotou Teachers College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Myostatin (MSTN) is a primary negative regulator of skeletal muscle mass and causes multiple metabolic changes. However, whether MSTN mutation affects heart morphology and physiology remains unclear. Myostatin mutation (MT) had no effect on cattle cardiac muscle in histological examination, but in biochemical assays, glycolysis increased in cattle hearts with MT. Compared with wild-type cattle, there were no differences in mRNA and protein levels of rate-limiting enzymes, but phosphofructokinase (PFK) phosphorylation increased in cattle hearts with MT. Transcriptome analysis showed that phosphodiesterase-5A (PDE5A), a target for inhibiting cGMP-PKG signaling, was downregulated. For the mechanism, chromatin immunoprecipitation qPCR showed that the SMAD2/SMAD3 complex in the canonical downstream pathway for MSTN combined with the promoter of PDE5A. The cGMP-PKG pathway was activated, and PKG increased phosphorylation of PFK in cattle hearts with MT. In addition, activation of PKG and the increase in PFK phosphorylation promoted glycolysis. Knockdown of PKG resulted in the opposite phenomena. The results indicated that MT potentiated PFK phosphorylation

Indexed as

glycolysisheartmyostatin mutationPDE5A-cGMP-PKGphosphofructokinase

Identifiers

PMID35155444
PMCPMC8831326
OpenAlexW4210799319

What OpenQuestion holds

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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 OpenQuestion graph.