Research progress on the correlation between estrogen and estrogen receptor on postmenopausal sarcopenia

肌萎缩 雌激素 雌激素受体 医学 绝经后妇女 雌激素受体α 内科学 内分泌学 生物信息学 生物 乳腺癌 癌症
作者
Chengmei Zhang,Xin Feng,Xue Zhang,Yu Chen,Juan Kong,Yan Lou
出处
期刊:Frontiers in Endocrinology [Frontiers Media]
卷期号:15 被引量:1
标识
DOI:10.3389/fendo.2024.1494972
摘要

Estrogen is a necessary sex steroid and potent neuroprotective hormone. It plays a multifaceted role beyond the reproductive system, extending its influence to the brain, skeletal muscle, and other organs. Estrogen's role in cognition, mood, autonomic regulation, and neuroprotection involves interactions with neurotransmitters, neuromodulators in a distributed manner. Notably, the impact of estrogen on mitochondrial metabolism in skeletal muscle is particularly significant due to a unique modulated bioenergetic profiles, synaptic plasticity, and neuronal health. The deficiency of estrogen in menopause has been linked to changes in brain structure, connectivity, energy metabolism. Therewith, these are crucial factors in cognitive function and the risk of Alzheimer's diseases. Besides, it leads to endocrine and metabolic dysfunction, resulting in osteoporosis, metabolic syndrome, and a tendency toward decreased muscle mass and strength. Estrogen's influence on mitochondrial function is particularly relevant to aging, as it affects the production of ATP and the overall metabolic health of the brain. Estrogen decline in women skeletal muscle mass is usually related to sarcopenia, a prevalent disease observed in vulnerable elderly individuals. Therefore, estrogen is considered to play a crucial role in skeletal muscle homeostasis and motor ability, although the exact mechanism remains unclear. This paper reviews the literature on the impact of estrogen on postmenopausal skeletal muscle diseases and the underlying molecular mechanisms, especially in terms of mitochondrial metabolism. In summary, estrogen plays an important role in the health of skeletal muscle in postmenopausal women, and its impact on mitochondrial function and homeostasis offers potential targets for the development of new strategies to treat sarcopenia.

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