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Formation of Muscle Fibers from Myoblasts01:13

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Related Experiment Video

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Skeletal Muscle Gender Dimorphism from Proteomics
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Co-Expression Transcriptomic Profiling Identifies Sex-Universal Molecular Markers of Muscle Atrophy.

Pingping Fu1, Fengfeng Wu1, Qinguang Xu1

  • 1Department of Rehabilitation Medicine, Huzhou Central Hospital, Fifth School of Clinical Medicine of Zhejiang Chinese Medical University, Huzhou, China.

IET Systems Biology
|October 11, 2025
PubMed
Summary
This summary is machine-generated.

Muscle disuse atrophy (MDA) involves gender-specific mechanisms. This study identified CD36 as a common biomarker and C21ORF33 as a male-specific biomarker for MDA, highlighting immune roles.

Keywords:
biomarkergender differencesimmune infiltrationmuscle disuse atrophy

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Area of Science:

  • Molecular Biology
  • Genomics
  • Immunology

Background:

  • Muscle disuse atrophy (MDA) is a significant health concern linked to inactivity.
  • Existing research often overlooks gender similarities and differences in MDA mechanisms.

Purpose of the Study:

  • To investigate gender-specific and common molecular mechanisms underlying muscle disuse atrophy.
  • To identify novel biomarkers for MDA across genders.

Main Methods:

  • Transcriptomic data analysis from the Gene Expression Omnibus database, stratified by gender.
  • Weighted gene co-expression network analysis (WGCNA) and Least Absolute Shrinkage and Selection Operator (LASSO) regression.
  • Immune cell infiltration analysis and biomarker validation in a mouse model.

Main Results:

  • CD36 identified as a potential pan-gender biomarker for MDA; C21ORF33 identified as a male-specific MDA biomarker.
  • WGCNA revealed gender-specific gene co-expression modules associated with MDA.
  • Immune dysregulation, including altered B cell and eosinophil populations, implicated in female MDA.

Conclusions:

  • CD36 and C21ORF33 show promise as diagnostic biomarkers for muscle disuse atrophy.
  • Chronic inflammation and immune dysregulation play critical roles in MDA pathogenesis.
  • The non-gender-specific role of CD36 suggests its fundamental importance in MDA.