期刊
FRONTIERS IN NEUROENDOCRINOLOGY
卷 55, 期 -, 页码 -出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.yfrne.2019.100787
关键词
Apoptosis; Autophagy; Brain plasticity; Cell signaling; Estrogen receptor; Excitotoxicity; Glia; Mitochondria; Neurogenesis; Neuroinflammation
资金
- Agencia Estatal de Investigacion [BFU2017-82754-R]
- CIBERFES
- Fondos FEDER
Estradiol, either from peripheral or central origin, activates multiple molecular neuroprotective and neuror eparative responses that, being mediated by estrogen receptors or by estrogen receptor independent mechanisms, are initiated at the membrane, the cytoplasm or the cell nucleus of neural cells. Estrogen-dependent signaling regulates a variety of cellular events, such as intracellular Ca2+ levels, mitochondrial respiratory capacity, ATP production, mitochondrial membrane potential, autophagy and apoptosis. In turn, these molecular and cellular actions of estradiol are integrated by neurons and non-neuronal cells to generate different tissue protective responses, decreasing blood-brain barrier permeability, oxidative stress, neuroinflammation and excitotoxicity and promoting synaptic plasticity, axonal growth, neurogenesis, remyelination and neuroregeneration. Recent findings indicate that the neuroprotective and neuroreparative actions of estradiol are different in males and females and further research is necessary to fully elucidate the causes for this sex difference.
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