Androgens as the “old age stick” in skeletal muscle
Abstract Aging is associated with a reduction in skeletal muscle fiber size and number, leading to a decline in physical function and structural integrity—a condition known as sarcopenia. This syndrome is further characterized by elevated levels of inflammatory mediators that promote skeletal muscle...
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| Format: | Article |
| Language: | English |
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BMC
2025-04-01
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| Series: | Cell Communication and Signaling |
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| Online Access: | https://doi.org/10.1186/s12964-025-02163-6 |
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| author | Giulia Gentile Ferdinando De Stefano Carmela Sorrentino Rosa D’Angiolo Carmine Lauretta Pia Giovannelli Antimo Migliaccio Gabriella Castoria Marzia Di Donato |
| author_facet | Giulia Gentile Ferdinando De Stefano Carmela Sorrentino Rosa D’Angiolo Carmine Lauretta Pia Giovannelli Antimo Migliaccio Gabriella Castoria Marzia Di Donato |
| author_sort | Giulia Gentile |
| collection | DOAJ |
| description | Abstract Aging is associated with a reduction in skeletal muscle fiber size and number, leading to a decline in physical function and structural integrity—a condition known as sarcopenia. This syndrome is further characterized by elevated levels of inflammatory mediators that promote skeletal muscle catabolism and reduce anabolic signaling. Androgens are involved in various biological processes, including the maintenance, homeostasis and trophism of skeletal muscle mass. The decline in androgen levels contributes, indeed, to androgen deficiency in aging people. Such clinical syndrome exacerbates the muscle loss and fosters sarcopenia progression. Nevertheless, the mechanism(s) by which the reduction in androgen levels influences sarcopenia risk and progression remains debated and the therapeutic benefits of androgen-based interventions are still unclear. Given the significant societal and economic impacts of sarcopenia, investigating the androgen/androgen receptor axis in skeletal muscle function is essential to enhance treatment efficacy and reduce healthcare costs. This review summarizes current knowledge on the role of male hormones and their-dependent signaling pathways in sarcopenia. We also highlight the cellular and molecular features of this condition and discuss the mechanisms by which androgens preserve the muscle homeostasis. The pros and cons of clinical strategies and emerging therapies aimed at mitigating muscle degeneration and aging-related decline are also presented. |
| format | Article |
| id | doaj-art-d394e498e2cc41269bf63fe3ac796ee7 |
| institution | Kabale University |
| issn | 1478-811X |
| language | English |
| publishDate | 2025-04-01 |
| publisher | BMC |
| record_format | Article |
| series | Cell Communication and Signaling |
| spelling | doaj-art-d394e498e2cc41269bf63fe3ac796ee72025-08-20T03:48:02ZengBMCCell Communication and Signaling1478-811X2025-04-0123111510.1186/s12964-025-02163-6Androgens as the “old age stick” in skeletal muscleGiulia Gentile0Ferdinando De Stefano1Carmela Sorrentino2Rosa D’Angiolo3Carmine Lauretta4Pia Giovannelli5Antimo Migliaccio6Gabriella Castoria7Marzia Di Donato8Department of Precision Medicine, University of Campania “Luigi Vanvitelli”Department of Precision Medicine, University of Campania “Luigi Vanvitelli”Department of Precision Medicine, University of Campania “Luigi Vanvitelli”Department of Precision Medicine, University of Campania “Luigi Vanvitelli”Department of Precision Medicine, University of Campania “Luigi Vanvitelli”Department of Precision Medicine, University of Campania “Luigi Vanvitelli”Department of Precision Medicine, University of Campania “Luigi Vanvitelli”Department of Precision Medicine, University of Campania “Luigi Vanvitelli”Department of Precision Medicine, University of Campania “Luigi Vanvitelli”Abstract Aging is associated with a reduction in skeletal muscle fiber size and number, leading to a decline in physical function and structural integrity—a condition known as sarcopenia. This syndrome is further characterized by elevated levels of inflammatory mediators that promote skeletal muscle catabolism and reduce anabolic signaling. Androgens are involved in various biological processes, including the maintenance, homeostasis and trophism of skeletal muscle mass. The decline in androgen levels contributes, indeed, to androgen deficiency in aging people. Such clinical syndrome exacerbates the muscle loss and fosters sarcopenia progression. Nevertheless, the mechanism(s) by which the reduction in androgen levels influences sarcopenia risk and progression remains debated and the therapeutic benefits of androgen-based interventions are still unclear. Given the significant societal and economic impacts of sarcopenia, investigating the androgen/androgen receptor axis in skeletal muscle function is essential to enhance treatment efficacy and reduce healthcare costs. This review summarizes current knowledge on the role of male hormones and their-dependent signaling pathways in sarcopenia. We also highlight the cellular and molecular features of this condition and discuss the mechanisms by which androgens preserve the muscle homeostasis. The pros and cons of clinical strategies and emerging therapies aimed at mitigating muscle degeneration and aging-related decline are also presented.https://doi.org/10.1186/s12964-025-02163-6AndrogensAndrogen receptorAgingSarcopenia |
| spellingShingle | Giulia Gentile Ferdinando De Stefano Carmela Sorrentino Rosa D’Angiolo Carmine Lauretta Pia Giovannelli Antimo Migliaccio Gabriella Castoria Marzia Di Donato Androgens as the “old age stick” in skeletal muscle Cell Communication and Signaling Androgens Androgen receptor Aging Sarcopenia |
| title | Androgens as the “old age stick” in skeletal muscle |
| title_full | Androgens as the “old age stick” in skeletal muscle |
| title_fullStr | Androgens as the “old age stick” in skeletal muscle |
| title_full_unstemmed | Androgens as the “old age stick” in skeletal muscle |
| title_short | Androgens as the “old age stick” in skeletal muscle |
| title_sort | androgens as the old age stick in skeletal muscle |
| topic | Androgens Androgen receptor Aging Sarcopenia |
| url | https://doi.org/10.1186/s12964-025-02163-6 |
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