Estrogen or oestrogen (see spelling differences) is the primary female sex hormone and is responsible for development and regulation of the female reproductive system and secondary sex characteristics. Estrogen may also refer to any substance, natural or synthetic that mimics the effects of the natural hormone.
The steroid 17β-estradiol is the most potent and prevalent endogenous estrogen, but several metabolites of estradiol also have estrogenic hormonal activity. Synthetic estrogens are used as part of some oral contraceptives, in estrogen replacement therapy for postmenopausal women, and in hormone replacement therapy for trans women.
Like all steroid hormones, estrogens readily diffuse across the cell membrane. Once inside the cell, they bind to and activate estrogen receptors (ERs) which in turn modulate the expression of many genes.Additionally, estrogens bind to and activate rapid-signaling membrane estrogen receptors (mERs),[ such as GPER (GPR30).
Estrogens are synthesized in all vertebrates as well as some insects.
Their presence in both vertebrates and insects suggests that estrogenic sex hormones have an ancient evolutionary history. Quantitatively, estrogens circulate at lower levels than androgens in both men and women.
Estrogens are known to play an important role in regulating bone homeostasis and preventing postmenopausal bone loss.
There is significant theoretical evidence for the potential role of estrogen and progesterone use in altering the pathogenesis of SAH. Nevertheless, this has received mixed reviews in both case controlled studies and cohort analysis within the literature 1)
Acute hydrocephalus is a common complication of subarachnoid hemorrhage (SAH). Data demonstrate that gender influences acute hydrocephalus development in a rat SAH model. Future studies should determine the role of estrogen in SAH-induced hydrocephalus 2).
Estrogen, specifically 17 β -estradiol (E2), has potential therapeutic implications for ameliorating the delayed neurological deterioration which follows aneurysmal subarachnoid hemorrhage SAH.
E2 potentiates vasodilation by activating endothelial nitric oxide synthase (eNOS), preventing increased inducible NOS (iNOS) activity caused by SAH, and decreasing endothelin-1 production. E2 provides neuroprotection by increasing thioredoxin expression, decreasing c-Jun N-terminal kinase activity, increasing neuroglobin levels, preventing SAH-induced suppression of the Akt signaling pathway, and upregulating the expression of adenosine A2a receptor. The net effect of E2 modulation of these various effectors is the promotion of neuronal survival, inhibition of apoptosis, and decreased oxidative damage and inflammation. E2 is a potentially potent therapeutic tool for improving outcomes related to post-SAH CV and DCI. However, clinical evidence supporting its benefits remains lacking. Given the promising preclinical data available, further studies utilizing E2 for the treatment of patients with ruptured intracranial aneurysms appear warranted 4).