Skeletal muscle wasting: The estrogen side of sexual dimorphism

Shawna L. McMillin, Everett C. Minchew, Dawn A. Lowe, Espen E. Spangenburg

Research output: Contribution to journalArticlepeer-review

4 Scopus citations


The importance of defining sex differences across various biological and physiological mechanisms is more pervasive now than it has been over the past 15-20 years. As the muscle biology field pushes to identify small molecules and interventions to prevent, attenuate, or even reverse muscle wasting, we must consider the effect of sex as a biological variable. It should not be assumed that a therapeutic will affect males and females with equal efficacy or equivalent target affinities under conditions where muscle wasting is observed. With that said, it is not surprising to find that we have an unclear or even a poor understanding of the effects of sex or sex hormones on muscle wasting conditions. Although recent investigations are beginning to establish experimental approaches that will allow investigators to assess the impact of sex-specific hormones on muscle wasting, the field still needs rigorous scientific tools that will allow the community to address critical hypotheses centered around sex hormones. The focus of this review is on female sex hormones, specifically estrogens, and the roles that these hormones and their receptors play in skeletal muscle wasting conditions. With the overall review goal of assembling the current knowledge in the area of sexual dimorphism driven by estrogens with an effort to provide insights to interested physiologists on necessary considerations when trying to assess models for potential sex differences in cellular and molecular mechanisms of muscle wasting.

Original languageEnglish (US)
Pages (from-to)C24-C37
JournalAmerican Journal of Physiology - Cell Physiology
Issue number1
StatePublished - Jan 1 2022

Bibliographical note

Funding Information:
This study was funded by National Institutes of Health Grants R61AR078100 and RO1AR066660 (to E.E.S.), RO1AG031743 and RO1AG062899 (to D.A.L.), and T32AR007612 (to S.L.M.).

Publisher Copyright:
© 2022 the American Physiological Society.


  • Cachexia
  • Disuse
  • Estradiol
  • Sarcopenia
  • Skeletal muscle

PubMed: MeSH publication types

  • Journal Article
  • Research Support, N.I.H., Extramural
  • Review


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