Evidence map›Paper›PMID 34283807›Full record

ArticleThe Journal of clinical investigation2021

IRE1α regulates skeletal muscle regeneration through Myostatin mRNA decay.

Shengqi He, Tingting Fu, Yue Yu, Qinhao Liang, Luyao Li, Jing Liu, Xuan Zhang, Qian Zhou, Qiqi Guo, Dengqiu Xu and 6 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.9field-weighted citation impact, top 8% 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

33 citing papers in PubMed, 51 citations in OpenAlex.

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  11. Listerin Alleviates Alzheimer's Disease through IRE1-mediated Decay of TLR4 mRNA.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  12. Review
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  19. Zfp697 is an RNA-binding protein that regulates skeletal muscle inflammation and remodeling.Proceedings of the National Academy of Sciences of the United States of America · 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

16 authors at 5 institutions in 2 countries.

Shengqi HeCollege of Life Sciences, Wuhan University, Wuhan, China.
Tingting FuModel Animal Research Center, Nanjing University, Nanjing, China.
Yue YuDepartment of Medicine, Beth Israel Deaconess Medical Center, Boston, United States of America.
Qinhao LiangCollege of Life Sciences, Wuhan University, Wuhan, China.
Luyao LiCollege of Life Sciences, Wuhan University, Wuhan, China.
Jing LiuModel Animal Research Center, Nanjing University, Nanjing, China.
Xuan ZhangCollege of Life Sciences, Wuhan University, Wuhan, China.
Qian ZhouModel Animal Research Center, Nanjing University, Nanjing, China.
Qiqi GuoModel Animal Research Center, Nanjing University, Nanjing, China.
Dengqiu XuModel Animal Research Center, Nanjing University, Nanjing, China.
Yong ChenCollege of Life Sciences, Wuhan University, Wuhan, China.
Xiaolong WangCollege of Animal Science and Technology, Northwest A&F University, Yangling, China.
Yulin ChenCollege of Animal Science and Technology, Northwest A&F University, Yangling, China.
Jianmiao LiuCellular Signaling Laboratory, Huazhong University of Science and Technology, Wuhan, China.
Zhenji GanModel Animal Research Center, Nanjing University, Nanjing, China.
Yong LiuCollege of Life Sciences, Wuhan University, Wuhan, China.
Wuhan University · CNNanjing Drum Tower Hospital · CNHuazhong Agricultural University · CNBeth Israel Deaconess Medical Center · USNorthwest A&F University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Skeletal muscle can undergo a regenerative process from injury or disease to preserve muscle mass and function, which is critically influenced by cellular stress responses. Inositol-requiring enzyme 1 (IRE1) is an ancient endoplasmic reticulum (ER) stress sensor and mediates a key branch of the unfolded protein response (UPR). In mammals, IRE1α is implicated in the homeostatic control of stress responses during tissue injury and regeneration. Here, we show that IRE1α serves as a myogenic regulator in skeletal muscle regeneration in response to injury and muscular dystrophy. We found in mice that IRE1α was activated during injury-induced muscle regeneration, and muscle-specific IRE1α ablation resulted in impaired regeneration upon cardiotoxin-induced injury. Gain- and loss-of-function studies in myocytes demonstrated that IRE1αacts to sustain both differentiation in myoblasts and hypertrophy in myotubes through regulated IRE1-dependent decay (RIDD) of mRNA encoding Myostatin, a key negative regulator of muscle repair and growth. Furthermore, in the mouse model of Duchenne muscular dystrophy (DMD), loss of muscle IRE1α resulted in augmented Myostatin signaling and exacerbated the dystrophic phenotypes. Thus, these results reveal a pivotal role for the RIDD output of IRE1α in muscle regeneration, offering new insight into potential therapeutic strategies for muscle loss diseases.

Indexed as

Cell stressMolecular pathologyMuscle BiologySkeletal muscle

Identifiers

PMID34283807
PMCPMC8409588
OpenAlexW3186337640

What OpenQuestion 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 OpenQuestion graph.