Estrogen receptor signaling and targets: Bones, breasts and brain (Review)

生物 雌激素受体 三苯氧胺 雌激素受体α 核受体 雌激素 芳香化酶 雌激素受体 信号转导 癌症研究 机制(生物学) 癌症 细胞生物学 乳腺癌 内分泌学 基因 遗传学 转录因子 认识论 哲学
作者
Meropi Toumba,Alexandros Kythreotis,Konstantina Panayiotou,Nicos Skordis
出处
期刊:Molecular Medicine Reports [Spandidos Publishing]
卷期号:30 (2) 被引量:4
标识
DOI:10.3892/mmr.2024.13268
摘要

Estrogens are involved in a number of physiological functions, including in the development of the brain, growth, reproduction and metabolism. The biological actions of estrogens are achieved by binding to estrogen receptors (ERs) in numerous types of tissues. ERα and ERβ belong to the nuclear receptor superfamily and the G‑protein coupled ER1 (GPER1) is a membrane receptor. The primary biologically active estrogen, 17β‑estradiol demonstrates a high affinity for ERs. Mechanistically, estrogens bind to the ERs in the nucleus, and the complex then dimerize and bind to estrogen response elements (EREs) located in the promoter regions of the target genes. This is referred to as the genomic mechanism of ERs' function. Furthermore, ERs can also act through kinases and other molecular interactions leading to specific gene expression and functions, referred to as the non‑genomic mechanism. While ERα and ERβ exert their functions via both genomic and non‑genomic pathways, GPER1 exerts its function primarily via the non‑genomic pathways. Any aberrations in ER signaling can lead to one of a number of diseases such as disorders of growth and puberty, fertility and reproduction abnormalities, cancer, metabolic diseases or osteoporosis. In the present review, a focus is placed on three target tissues of estrogens, namely the bones, the breasts and the brain, as paradigms of the multiple facets of the ERs. The increasing prevalence of breast cancer, particularly hormone receptor‑positive breast cancer, is a challenge for the development of novel antihormonal therapies other than tamoxifen and aromatase inhibitors, to minimize toxicity from the long treatment regimens in patients with breast cancer. A complete understanding of the mechanism of action of ERs in bones may highlight options for novel targeted treatments for osteoporosis. Likewise, the aging of the brain and related diseases, such as dementia and depression, are associated with a lack of estrogen, particularly in women following menopause. Furthermore, gender dysphoria, a discordance between experienced gender and biological sex, is commonly hypothesized to emerge due to discrepancies in cerebral and genital sexual differentiation. The exact role of ERs in gender dysphoria requires further research.
最长约 10秒,即可获得该文献文件

科研通智能强力驱动
Strongly Powered by AbleSci AI
科研通是完全免费的文献互助平台,具备全网最快的应助速度,最高的求助完成率。 对每一个文献求助,科研通都将尽心尽力,给求助人一个满意的交代。
实时播报
Master发布了新的文献求助10
刚刚
ZZ发布了新的文献求助10
1秒前
jenningseastera应助duduguai采纳,获得10
2秒前
2秒前
闪闪落雁完成签到,获得积分10
4秒前
文天发布了新的文献求助10
4秒前
5秒前
Agan完成签到,获得积分10
8秒前
zhhh发布了新的文献求助10
8秒前
Djo完成签到,获得积分10
9秒前
斯文败类应助难过盼海采纳,获得10
12秒前
13秒前
Flame完成签到,获得积分10
15秒前
小朱完成签到,获得积分10
17秒前
小唐发布了新的文献求助10
18秒前
Flame发布了新的文献求助10
20秒前
胖虎爱睡觉完成签到,获得积分10
24秒前
25秒前
Dian完成签到,获得积分10
27秒前
28秒前
29秒前
ZZ完成签到,获得积分20
30秒前
31秒前
32秒前
难过盼海发布了新的文献求助10
33秒前
Eleven完成签到,获得积分10
33秒前
yasen发布了新的文献求助10
34秒前
JamesPei应助活力酒窝采纳,获得10
34秒前
36秒前
充电宝应助虚拟的惜筠采纳,获得10
37秒前
李振华完成签到,获得积分20
38秒前
大方元风发布了新的文献求助30
38秒前
THEO发布了新的文献求助10
38秒前
蔡蔡蔡发布了新的文献求助10
41秒前
小马甲应助薄荷味采纳,获得10
41秒前
花景铭完成签到,获得积分10
41秒前
42秒前
科目三应助大成子采纳,获得10
42秒前
田様应助难过盼海采纳,获得10
42秒前
43秒前
高分求助中
【此为提示信息,请勿应助】请按要求发布求助,避免被关 20000
Technologies supporting mass customization of apparel: A pilot project 450
Mixing the elements of mass customisation 360
Периодизация спортивной тренировки. Общая теория и её практическое применение 310
the MD Anderson Surgical Oncology Manual, Seventh Edition 300
Nucleophilic substitution in azasydnone-modified dinitroanisoles 300
Political Ideologies Their Origins and Impact 13th Edition 260
热门求助领域 (近24小时)
化学 材料科学 医学 生物 工程类 有机化学 物理 生物化学 纳米技术 计算机科学 化学工程 内科学 复合材料 物理化学 电极 遗传学 量子力学 基因 冶金 催化作用
热门帖子
关注 科研通微信公众号,转发送积分 3781669
求助须知:如何正确求助?哪些是违规求助? 3327234
关于积分的说明 10230111
捐赠科研通 3042093
什么是DOI,文献DOI怎么找? 1669791
邀请新用户注册赠送积分活动 799335
科研通“疑难数据库(出版商)”最低求助积分说明 758774