Evidence map›Paper›PMID 37288303›Full record

ReviewFrontiers in endocrinology2023

Myostatin: a potential therapeutic target for metabolic syndrome.

Ming Yang, Chongbin Liu, Na Jiang, Yan Liu, Shilu Luo, Chenrui Li, Hao Zhao, Yachun Han, Wei Chen, Li Li and 2 more

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in endocrinology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
4.0field-weighted citation impact, top 6% 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

26 citing papers in PubMed, 26 citations in OpenAlex.

  1. Review
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  4. Article
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  6. Review
  7. Review
  8. Article
  9. Inflammation-Insulin Resistance Crosstalk and the Central Role of Myokines.International journal of molecular sciences · 2025
    Review
  10. Review
  11. Article
  12. Review
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  16. Loss ofVeterinary sciences · 2025
    Article
  17. 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

12 authors at 3 institutions in 1 country.

Ming YangDepartment of Nephrology, The Second Xiangya Hospital of Central South University, Changsha, China.
Chongbin LiuDepartment of Nephrology, The Second Xiangya Hospital of Central South University, Changsha, China.
Na JiangDepartment of Nephrology, The Second Xiangya Hospital of Central South University, Changsha, China.
Yan LiuDepartment of Nephrology, The Second Xiangya Hospital of Central South University, Changsha, China.
Shilu LuoDepartment of Nephrology, The Second Xiangya Hospital of Central South University, Changsha, China.
Chenrui LiDepartment of Nephrology, The Second Xiangya Hospital of Central South University, Changsha, China.
Hao ZhaoDepartment of Nephrology, The Second Xiangya Hospital of Central South University, Changsha, China.
Yachun HanDepartment of Nephrology, The Second Xiangya Hospital of Central South University, Changsha, China.
Wei ChenDepartment of Nephrology, The Second Xiangya Hospital of Central South University, Changsha, China.
Li LiDepartment of Nephrology, The Second Xiangya Hospital of Central South University, Changsha, China.
Li XiaoDepartment of Nephrology, The Second Xiangya Hospital of Central South University, Changsha, China.
Lin SunDepartment of Nephrology, The Second Xiangya Hospital of Central South University, Changsha, China.
Soil and Fertilizer Institute of Hunan Province · CNCentral South University · CNSecond Xiangya Hospital of Central South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Metabolic syndrome is a complex metabolic disorder, its main clinical manifestations are obesity, hyperglycemia, hypertension and hyperlipidemia. Although metabolic syndrome has been the focus of research in recent decades, it has been proposed that the occurrence and development of metabolic syndrome is related to pathophysiological processes such as insulin resistance, adipose tissue dysfunction and chronic inflammation, but there is still a lack of favorable clinical prevention and treatment measures for metabolic syndrome. Multiple studies have shown that myostatin (MSTN), a member of the TGF-β family, is involved in the development and development of obesity, hyperlipidemia, diabetes, and hypertension (clinical manifestations of metabolic syndrome), and thus may be a potential therapeutic target for metabolic syndrome. In this review, we describe the transcriptional regulation and receptor binding pathway of MSTN, then introduce the role of MSTN in regulating mitochondrial function and autophagy, review the research progress of MSTN in metabolic syndrome. Finally summarize some MSTN inhibitors under clinical trial and proposed the use of MSTN inhibitor as a potential target for the treatment of metabolic syndrome.

Indexed as

Insulin ResistanceMetabolic SyndromeHumansMuscle, SkeletalMyostatinObesityMyostatindiabeteslipidmetabolic syndromemyostatinobesity

Identifiers

PMID37288303
PMCPMC10242177
OpenAlexW4378085175

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.