Project description:Women’s aging is characterized by menopausal loss of ovarian function, which has been suggested as a contributing factor to aging-related muscle deterioration and predisposes to the metabolic dysfunctions. However, the underlying molecular mechanisms have remained unknown. To identify mechanisms, we utilized muscle samples from 24 pre- and postmenopausal women, established proteome-wide profiles and identified upstream regulators and downstream cellular pathways associated with the differences in age, menopausal status and use of hormone replacement therapy (HRT). None of the premenopausal women used hormonal medication while the postmenopausal women were monozygotic twin-sister pairs who were either current HRT users or had never used HRT. The proteomic analyses resulted in the quantification of 762 muscle proteins of which 158 were for the first time associated with female muscle aging. The Ingenuity Pathway Analysis pinpointed 17β-estradiol as a potential upstream regulator of the observed differences in the major downstream pathways including dysregulated cell death and glycolysis pathways. The results increase knowledge on the factors related to skeletal muscle signaling and aging. This is of importance, since the role of female sex hormones in the regulation of muscle cell signaling has been under appreciated and scarcely studied as compared to vast amount of data on male sex hormones and skeletal muscle. Our results clearly demonstrate the also female sex hormones and HRT should be considered as potential active players and an intervention targets to promote women’s muscular health.

2017-09-12 | PXD006446 | Pride

Homo sapiens

Project description:Human skeletal muscle

| PRJNA85385 | ENA